A 75-year-old woman with chest pain and transient severe left ventricular systolic dysfunction | Revista Portuguesa de Cardiologia (English edition)

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A 40% luminal stenosis with no evidence of plaque rupture or thrombus was observed in the left anterior descending artery. The circumflex and right coronary arteries were normal." ] ] ] "textoCompleto" => "Case reportA 75-year-old woman with a history of hypertension and aortic valve replacement with a mechanical prosthesis ten years earlier presented to the emergency room (ER) with acute-onset chest pain and diaphoresis. She described a three-month history of chest pain episodes of short duration with no clear relation with effort with no peripheral edemas or orthopnea.On initial evaluation, the patient reported intense chest pressure but was not in acute distress. She was afebrile, with blood pressure 72/44 mmHg, heart rate 110 beats/min, and respiratory rate 32 breaths/min; pulse oximetry revealed oxygen saturation of 94% in room air. Chest auscultation revealed regular prosthetic sounds with a systolic murmur; rales were heard in both lung fields. The abdominal examination was unremarkable. Her lower extremities were pale and cold but showed no edema. The remainder of the physical examination was normal.The patient's hypotension and tachycardia suggested the early stages of shock and thus warranted urgent diagnostic testing and management, particularly in a patient with chest pressure. Her hypertension increased the likelihood of an acute coronary syndrome or aortic dissection. The systolic murmur may have been related to prosthetic valve dysfunction or to a mechanical complication of myocardial infarction, such as ventricular septal rupture or papillary muscle rupture, causing acute mitral regurgitation.A 12-lead electrocardiogram (ECG), obtained approximately six hours after the onset of chest pressure, revealed normal sinus rhythm with widespread ST-segment depression (1–2 mm in leads V2 to V6, DI and aVl, DII–III and aVF) (<a class="elsevierStyleCrossRef" href="#fig0005">Figure 1</a>A).<elsevierMultimedia ident="fig0005"></elsevierMultimedia>The electrocardiographic findings were consistent with myocardial ischemia, but other conditions associated with ST-segment depression and mimicking myocardial ischemia also had to be considered. An echocardiogram can help with differential diagnosis by identifying regional wall motion abnormalities, a native or prosthetic valve disorder, pericardial effusion, mechanical complications of acute myocardial infarction (as noted above), or even proximal aortic disease.Transthoracic echocardiography performed in the ER revealed global hypokinesis and impaired left ventricular function with severely depressed ejection fraction (EF); there were no signs of prosthesis dysfunction and the peak gradient between aortic and left ventricular systolic pressures was 26 mmHg.The patient became progressively less responsive, her blood pressure decreased and metabolic acidosis (pH 7.33, PaCO2 23.3 mmHg, HCO3 12.1 mmol/l and base excess −13.8) ensued. In the presence of signs of shock, most probably for cardiocirculatory causes, dobutamine and noradrenaline were initiated.The patient was also given aspirin 250 mg orally, and clopidogrel 600 mg orally. Her INR was 3.6.Laboratory results were as follows: hemoglobin 11.1 g/dl, platelet count 190000/ml, white-cell count 10300/ml, serum creatinine 0.7 mg/dl, blood glucose 106 mg/dl, creatine kinase 135 IU/dl, creatine kinase MB isoenzyme 14.1 ng/ml, and serum troponin I 1.43 ng/ml.Mildly elevated cardiac biomarkers confirmed myocardial injury but were inconsistent with chest pain six hours after clinical onset. These levels were somewhat unexpected and suggested either spontaneous intermittent coronary reperfusion throughout the day or another cardiovascular condition, such as apical ballooning syndrome, myocarditis or pulmonary embolism.Preparations were made for transfer to a hospital where percutaneous coronary intervention (PCI) could be carried out. On the patient's arrival at the PCI-capable hospital, her chest pressure had improved but was not completely resolved; her blood pressure was 118/61 mmHg and heart rate 97 beats/min.Coronary angiography revealed a 40% luminal stenosis in the left anterior descending artery (LAD) with no evidence of plaque rupture or thrombus (<a class="elsevierStyleCrossRef" href="#fig0010">Figure 2</a>A). Left ventriculography showed global hypokinesia with only mildly reduced left ventricular EF.<elsevierMultimedia ident="fig0010"></elsevierMultimedia>The patient was transferred to the cardiac intensive care unit. Aspirin therapy was continued and treatment with a statin was started. The chest pain and electrocardiographic ST depression resolved overnight (<a class="elsevierStyleCrossRef" href="#fig0005">Figure 1</a>B), and cardiac biomarker levels decreased from the peak values noted at admission. She was conscious and afebrile; her blood pressure rose, heart rate and urine output were normal, and she was weaned from inotropic support.The patient remained stable and the repeated transthoracic echocardiogram showed normal dimensions of the cardiac chambers and normally functioning aortic prosthesis, with a maximum gradient between aortic and left ventricular systolic pressures of 20 mmHg. No wall motion abnormalities were seen and EF was 48% (<a class="elsevierStyleCrossRef" href="#fig0015">Figure 3</a>A and B). To better assess the aortic prosthesis, a transesophageal echocardiogram was performed, which provided no additional information (<a class="elsevierStyleCrossRef" href="#fig0015">Figure 3</a>C and D).<elsevierMultimedia ident="fig0015"></elsevierMultimedia>During hospitalization there was no recurrence of pain, and a final diagnosis of non-ST elevation acute myocardial infarction was made; it was hypothesized that a thrombus formed on the LAD plaque could have transiently limited coronary blood flow. She was discharged home after six days of hospitalization on medication with aspirin 100 mg once daily, warfarin, atorvastatin 40 mg once daily, bisoprolol 2.5 mg once daily, and transcutaneous nitroglycerin 5 mg 12 hours a day. Cardiac contrast-enhanced magnetic resonance imaging (cMRI) was scheduled for two weeks later which revealed inferoseptal transmural infarct scar, inferior and inferolateral subendocardial infarct and mid-basal ischemia in the anterior and anterolateral walls (<a class="elsevierStyleCrossRef" href="#fig0020">Figure 4</a>).<elsevierMultimedia ident="fig0020"></elsevierMultimedia>One month after discharge, the patient was readmitted to the cardiac intensive care unit because of recurrent chest pain with hemodynamic instability; her blood pressure was 70/44 mmHg and her heart rate was 125 bpm. Marked ST depression in all precordial leads and severe global left ventricular dysfunction were present (<a class="elsevierStyleCrossRef" href="#fig0005">Figure 1</a>C).Despite her arterial hypotension, intravenous nitroglycerin was initiated with relief of chest pain, ST-T segment normalization and increase in blood pressure. Aspirin and bisoprolol were stopped and she was started on diltiazem 200 mg bid orally. After adequate informed consent had been obtained, pharmacological provocation testing for coronary artery spasm was performed with intracoronary injection of acetylcholine (ACh). After control coronary angiography, ACh was administered in a stepwise manner into the LAD (20–100 μg) and the right coronary artery (RCA) (20–50 μg) over a period of 20 seconds with a 3–5 min interval between injections. Coronary angiography was performed after each injection of ACh and when chest pain and/or ST changes were observed. At baseline coronary angiography showed no new stenosis or coronary blood flow impairment; after ACh injection into the LAD chest pain, ST-segment depression, LAD TIMI blood flow of 1 and transient grade 3 atrioventricular (AV) block were documented. Intracoronary administration of nitrates reversed the coronary spasm and AV conduction disturbances. Twenty minutes later, chest pain and ischemic ST changes recurred; response to nitrate infusion was poor and cardiac arrest with pulseless electrical activity occurred. Advanced life support was maintained for 32 minutes without return of spontaneous circulation.Clinical and angiographic diagnosisVasospastic angina (left anterior descending coronary artery spasm).DiscussionCoronary artery spasm is one of the important functional abnormalities of the coronary arteries and plays a significant role in the pathogenesis of a wide variety of ischemic heart disease and arrhythmic events. Provocative testing for coronary artery spasm is useful for the diagnosis of vasospastic angina (VSA). However, these tests are thought to have a potential risk of irreversible ischemia and arrhythmic complications.Definition and pathology of vasospastic anginaVSA is a condition in which a relatively large coronary artery transiently exhibits abnormal contraction. The initial description of VSA considered vasomotor instability as a key mechanism.<a class="elsevierStyleCrossRef" href="#bib0070">1</a> Prinzmetal et al. described a variant form of angina, which was later confirmed to be coronary spasm, and characterized by symptoms at rest (not during exertion) with ST elevation (not depression) on the ECG; it usually occurs in the early hours of the morning during depressed vagal tone and is associated with occlusion or near occlusion (>90% stenosis) of a focal proximal coronary segment on angiography.<a class="elsevierStyleCrossRef" href="#bib0075">2</a> Currently, it is accepted that both ST-segment elevation and depression can occur. In cases of a coronary artery completely or nearly completely occluded by spasm, transmural ischemia can occur and in turn cause anginal attacks with ST elevation on the ECG. However, if a coronary artery is partially occluded or diffusely narrowed by spasm, or if it is completely occluded by spasm but sufficient collateral flow has developed distally, nontransmural ischemia occurs, causing anginal attacks with ST depression on the ECG.<a class="elsevierStyleCrossRefs" href="#bib0080">3,4</a>The precise mechanism responsible for coronary spasm remains largely unknown; evidence suggests that the pathogenesis of coronary spasm differs from that of coronary atherosclerosis-based stenosis. Previous studies described different patterns of angiographic changes during the provocation test, including focal and diffuse spasm.<a class="elsevierStyleCrossRefs" href="#bib0080">3–5</a> The diffuse spasm pattern is reported to be more common in Japanese than Caucasian patients (20% vs. 7%).<a class="elsevierStyleCrossRefs" href="#bib0095">6,7</a> The focal spasm pattern is more frequently associated with a thicker coronary artery intima-media layer than the diffuse pattern and is induced in a setting of relatively advanced atherosclerotic lesions.<a class="elsevierStyleCrossRef" href="#bib0105">8</a> Older age, current smoking, high levels of high-sensitivity C-reactive protein, and elevated serum levels of remnant lipoprotein have been also identified as significant risk factors for VSA.<a class="elsevierStyleCrossRefs" href="#bib0110">9–11</a>Diagnostic criteriaCurrent guidelines from the European Society of Cardiology<a class="elsevierStyleCrossRef" href="#bib0125">12</a> and the American Heart Association/American College of Cardiology<a class="elsevierStyleCrossRef" href="#bib0130">13</a> hardly address the issue of VSA diagnosis and treatment since no large-scale clinical studies of this condition have been performed. The scientific committee of the Japanese Circulation Society (JCS)<a class="elsevierStyleCrossRef" href="#bib0085">4</a> has drawn up guidelines on the diagnosis and treatment of VSA. A flowchart for the diagnosis of VSA proposed by the JCS is illustrated in <a class="elsevierStyleCrossRef" href="#fig0025">Figure 5</a>.<elsevierMultimedia ident="fig0025"></elsevierMultimedia>According to the JCS guidelines, VSA is considered definite if the patient has clearly ischemic changes on the ECG during typical attacks, or a positive non-drug-induced coronary spasm provocation test (e.g. hyperventilation or exercise test), or a positive drug-induced coronary spasm provocation test (e.g. acetylcholine or ergonovine provocation test). The patient is considered to have suspected VSA when the ischemic changes on the ECG during attacks are borderline and no clear finding of myocardial ischemia or coronary spasm is obtained in any examination. VSA is considered unlikely if ischemic changes were absent on the ECG or the ECG was not performed during the attack and none of the previous conditions was present.Pharmacological provocation testing performed during coronary angiography is recommended in patients in whom VSA is suspected based on symptoms, but who have not been diagnosed with coronary spasm by non-invasive evaluation. It is contraindicated in patients considered at high risk of suffering a life-threatening complication of induced coronary spasm (e.g. patients with left main coronary trunk lesions, multivessel disease or untreated congestive heart failure).<a class="elsevierStyleCrossRef" href="#bib0085">4</a>Usefulness and safety of provocative testsPharmacological (i.e. ergonovine or ACh) and non-pharmacological (i.e. hyperventilation) provocation tests of coronary spasm during coronary angiography are established as a useful tool for the diagnosis of VSA, because coronary spasm develops transiently and it is not easy to document spontaneous attacks in a clinical context. The first provocation test with ergonovine during coronary angiography was performed at the Cleveland Clinic in 1973.<a class="elsevierStyleCrossRef" href="#bib0070">1</a> Subsequently Specchia et al. and Yasue et al. reported the use of ACh for the induction of coronary spasm.The intracoronary injection of ACh is known to have high sensitivity (90%) and specificity (99%) for the diagnosis of VSA; however, these tests are thought to have a potential risk of serious complications, including ventricular tachycardia (VT), ventricular fibrillation (VF), and bradyarrhythmias.<a class="elsevierStyleCrossRef" href="#bib0070">1</a> Recently, the safety and clinical implications of provocation tests were evaluated in a total of 1244 VSA patients from the nationwide multicenter registry of the Japanese Coronary Spasm Association.<a class="elsevierStyleCrossRef" href="#bib0095">6</a> The provocation tests were performed with either ACh (57%) or ergonovine (40%), and VT/VF and bradyarrhythmias developed in 3.2% and 2.7%, respectively. Overall, the incidence of arrhythmic complications was 6.8%, a comparable incidence to that during spontaneous angina attack (7.0%). Multivariate logistic regression analysis demonstrated that diffuse RCA spasm and the use of ACh had a significant correlation with provocation-related VT/VF. Mixed (focal plus diffuse)-type multivessel spasm had an important association with major adverse cardiac events in multivariate Cox proportional hazard regression analysis (adjusted hazard ratio, 2.84; 95% confidence interval 1.34–6.03, p<0.01), whereas provocation-related arrhythmias did not. The authors concluded that provocation tests have an acceptable level of safety and usefully information for the risk prediction of VSA patients. A previous study indicated that baseline QT dispersion was significantly greater in VSA patients complicated by ventricular arrhythmias. Slower infusion of provocation agents may reduce the incidence of arrhythmic complications, although excessively slow infusion of ACh may also lead to underestimation of the prevalence of coronary spasm.Conclusions and areas of uncertaintyThe use of provocation tests for the detection of abnormal coronary vasomotion in patients with anginal symptoms but angiographically unobstructed coronary arteries not only provides reassurance to the patient that a cause for the symptoms has been found, but also enables the physician to initiate appropriate medical therapy (calcium channel blockers and nitrates) aimed at reducing morbidity and mortality. This may also have important implications for healthcare systems, because most healthcare-related costs in patients with unobstructed coronary arteries are due to recurrent or ongoing angina pectoris. Although rare, the risks of provocation tests are potentially fatal and they should be avoided in patients with left main disease, multivessel disease, severe left ventricular dysfunction, or acute heart failure. Future studies are needed to assess the safety and effectiveness of intracoronary ACh provocation testing in a contemporary cohort of Caucasian patients with unobstructed coronary arteries.Ethical disclosuresProtection of human and animal subjectsThe authors declare that no experiments were performed on humans or animals for this study.Confidentiality of dataThe authors declare that they have followed the protocols of their work center on the publication of patient data.Right to privacy and informed consentThe authors have obtained the written informed consent of the patients or subjects mentioned in the article. The corresponding author is in possession of this document.FundingThis work has no funding.Conflicts of interestThe authors have no conflicts of interest to declare." "textoCompletoSecciones" => array:1 [ "secciones" => array:12 [ 0 => array:3 [ "identificador" => "xres817843" "titulo" => "Abstract" "secciones" => array:3 [ 0 => array:2 [ "identificador" => "abst0005" "titulo" => "Introduction" ] 1 => array:2 [ "identificador" => "abst0010" "titulo" => "Case report" ] 2 => array:2 [ "identificador" => "abst0015" "titulo" => "Conclusions" ] ] ] 1 => array:2 [ "identificador" => "xpalclavsec814951" "titulo" => "Keywords" ] 2 => array:3 [ "identificador" => "xres817842" "titulo" => "Resumo" "secciones" => array:3 [ 0 => array:2 [ "identificador" => "abst0020" "titulo" => "Introdução" ] 1 => array:2 [ "identificador" => "abst0025" "titulo" => "Descrição do caso" ] 2 => array:2 [ "identificador" => "abst0030" "titulo" => "Conclusão" ] ] ] 3 => array:2 [ "identificador" => "xpalclavsec814950" "titulo" => "Palavras-chave" ] 4 => array:2 [ "identificador" => "sec0005" "titulo" => "Case report" ] 5 => array:2 [ "identificador" => "sec0010" "titulo" => "Clinical and angiographic diagnosis" ] 6 => array:3 [ "identificador" => "sec0015" "titulo" => "Discussion" "secciones" => array:3 [ 0 => array:2 [ "identificador" => "sec0020" "titulo" => "Definition and pathology of vasospastic angina" ] 1 => array:2 [ "identificador" => "sec0025" "titulo" => "Diagnostic criteria" ] 2 => array:2 [ "identificador" => "sec0030" "titulo" => "Usefulness and safety of provocative tests" ] ] ] 7 => array:2 [ "identificador" => "sec0035" "titulo" => "Conclusions and areas of uncertainty" ] 8 => array:3 [ "identificador" => "sec0040" "titulo" => "Ethical disclosures" "secciones" => array:3 [ 0 => array:2 [ "identificador" => "sec0045" "titulo" => "Protection of human and animal subjects" ] 1 => array:2 [ "identificador" => "sec0050" "titulo" => "Confidentiality of data" ] 2 => array:2 [ "identificador" => "sec0055" "titulo" => "Right to privacy and informed consent" ] ] ] 9 => array:2 [ "identificador" => "sec0060" "titulo" => "Funding" ] 10 => array:2 [ "identificador" => "sec0065" "titulo" => "Conflicts of interest" ] 11 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "fechaRecibido" => "2014-12-08" "fechaAceptado" => "2015-03-10" "PalabrasClave" => array:2 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec814951" "palabras" => array:4 [ 0 => "Chest pain" 1 => "Acute heart failure" 2 => "Vasospastic angina" 3 => "Provocative test with acetylcholine" ] ] ] "pt" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palavras-chave" "identificador" => "xpalclavsec814950" "palabras" => array:4 [ 0 => "Dor torácica" 1 => "Insuficiência cardíaca aguda" 2 => "Angina vasospástica" 3 => "Testes de provocação com acetilcolina" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "en" => array:3 [ "titulo" => "Abstract" "resumen" => "IntroductionCoronary spasm can cause myocardial ischemia and angina in both patients with and without obstructive coronary artery disease. However, provocation tests using intracoronary acetylcholine (ACh) have been rarely performed in the Western world. Case reportWe report a case of a 75-year-old woman with a history of hypertension and a mechanical aortic prosthesis who presented in the emergency room with acute-onset chest pain, widespread ST-segment depression and severe left ventricular systolic dysfunction, with no signs of prosthesis dysfunction. Emergent coronary angiography excluded obstructive coronary artery disease. Pain relief and normalization of ST segment and systolic function occurred within six hours. The patient was treated for a possible thromboembolic myocardial infarction and was discharged home asymptomatic. Two weeks later, cardiac magnetic resonance was performed showing inferoseptal transmural infarct scar, inferior and inferolateral subendocardial infarct and mid-basal ischemia in the anterior and anterolateral walls. She was readmitted with recurrence of chest pain and it was decided to perform a provocation test with ACh. After injection of ACh into the left anterior descending artery, chest pain, ST-segment depression, blood flow impairment (TIMI 1) and transient grade 3 atrioventricular (AV) block occurred. Intracoronary administration of nitrates reversed the coronary spasm and AV conduction disturbances. Twenty minutes later, chest pain and ischemic ST changes recurred; there was no response to vasodilators and the patient developed cardiac arrest with pulseless electrical activity. Advanced life support was maintained for 32 minutes without return of spontaneous circulation. ConclusionsProvocation tests have a high sensitivity and specificity for the diagnosis of vasospastic angina. Although it is rare, these tests have the potential risk of irreversible spasm leading to arrhythmia and death." "secciones" => array:3 [ 0 => array:2 [ "identificador" => "abst0005" "titulo" => "Introduction" ] 1 => array:2 [ "identificador" => "abst0010" "titulo" => "Case report" ] 2 => array:2 [ "identificador" => "abst0015" "titulo" => "Conclusions" ] ] ] "pt" => array:3 [ "titulo" => "Resumo" "resumen" => "IntroduçãoO espasmo coronário pode causar isquemia miocárdica e angina em doentes com e sem doença coronária obstrutiva. Contudo, os testes de provocação com administração intracoronária de acetilcolina (ACh) têm sido raramente usados no mundo ocidental. Descrição do casoMulher de 75 anos com hipertensão arterial e prótese mecânica aórtica admitida no serviço de urgência por dor torácica aguda, depressão generalizada do segmento ST e disfunção sistólica grave do ventrículo esquerdo sem evidência de disfunção protésica. Realizámos angiografia coronária emergente que excluiu doença coronária obstrutiva. Seis horas após admissão, a dor, as alterações de ST e a disfunção ventricular normalizaram. Foi tratado como possível enfarte do miocárdio tromboembólico e teve alta assintomática. Duas semanas após, realizámos ressonância magnética cardíaca que mostrou cicatriz de enfarte transmural inferoseptal e de enfarte subendocárdico inferior e inferolateral, e isquemia anterior e ântero-lateral. A doente foi readmitida pela mesma sintomatologia e decidimos realizar estudo de provocação com ACh. Após a injeção de ACh na artéria descendente anterior documentámos dor torácica, depressão do segmento-ST, compromisso do fluxo (TIMI 1) e bloqueio atrioventricular (AV) completo. A administração intracoronária de nitratos reverteu o espasmo coronário e a perturbação da condução AV. No entanto, 20 minutos depois, houve recorrência de dor e alterações de ST sem resposta aos vasodilatadores evoluindo a doente para atividade elétrica sem pulso. Mantivemos suporte avançado de vida durante 32 minutos sem recuperação da circulação espontânea. ConclusãoOs testes de provocação têm elevada sensibilidade e especificidade para o diagnóstico de angina vasospática. Apesar de raro, estes testes também podem levar ao espasmo coronário irreversível, arritmia e morte." "secciones" => array:3 [ 0 => array:2 [ "identificador" => "abst0020" "titulo" => "Introdução" ] 1 => array:2 [ "identificador" => "abst0025" "titulo" => "Descrição do caso" ] 2 => array:2 [ "identificador" => "abst0030" "titulo" => "Conclusão" ] ] ] ] "multimedia" => array:5 [ 0 => array:7 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 3800 "Ancho" => 2477 "Tamanyo" => 1356552 ] ] "descripcion" => array:1 [ "en" => "(A–C) Electrocardiography. A 12-lead electrocardiogram obtained six hours after onset of chest pressure revealed normal sinus rhythm with widespread ST-segment depression (1–2 mm in leads V2 to V6, DI and aVl, DII–III and aVF) (A); the chest pain and ST-segment depression resolved (B); the patient was readmitted with recurrence of chest pain and marked ST depression in all precordial leads (C)." ] ] 1 => array:7 [ "identificador" => "fig0010" "etiqueta" => "Figure 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 1507 "Ancho" => 3038 "Tamanyo" => 296922 ] ] "descripcion" => array:1 [ "en" => "Coronary angiography. A 40% luminal stenosis with no evidence of plaque rupture or thrombus was observed in the left anterior descending artery. The circumflex and right coronary arteries were normal." ] ] 2 => array:7 [ "identificador" => "fig0015" "etiqueta" => "Figure 3" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr3.jpeg" "Alto" => 2237 "Ancho" => 3311 "Tamanyo" => 773129 ] ] "descripcion" => array:1 [ "en" => "(A–D) Echocardiography. Transthoracic echocardiogram performed after pain relief showed mean gradient between the aortic and left ventricular systolic pressures of 26 mmHg (A) and slightly impaired left ventricular systolic function with left ventricular ejection fraction of 49% using the three-dimensional Simpson's method (B); transesophageal echocardiography allowed better characterization of the mechanical aortic prosthesis, excluding valve dysfunction (C and D)." ] ] 3 => array:7 [ "identificador" => "fig0020" "etiqueta" => "Figure 4" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr4.jpeg" "Alto" => 2319 "Ancho" => 3180 "Tamanyo" => 737025 ] ] "descripcion" => array:1 [ "en" => "(A–G) Cardiac magnetic resonance imaging. Late-enhancement gadolinium evaluation showed transmural infarct scar in the inferoseptal wall and subendocardial infarct in the inferior and inferolateral walls (A–D). Ischemia (reversible perfusion defect) was documented in the mid-basal segments of the anterior and anterolateral walls (E–G)." ] ] 4 => array:7 [ "identificador" => "fig0025" "etiqueta" => "Figure 5" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr5.jpeg" "Alto" => 1579 "Ancho" => 2505 "Tamanyo" => 401679 ] ] "descripcion" => array:1 [ "en" => "Flowchart for the diagnosis of vasospastic angina (VSA). VSA can be diagnosed when anginal attacks disappear quickly upon administration of nitroglycerin, and at least one of the following reference items is present: (1) attacks appear at rest, particularly between night and early morning; (2) marked diurnal variation is observed in exercise tolerance (in particular, reduction of exercise capacity in the early morning); (3) attacks are accompanied by ST elevation on the ECG; (4) attacks are induced by hyperventilation (hyperpnea); (5) attacks are suppressed by calcium channel blockers but not by beta-blockers. VSA is considered definite if the patient has clearly ischemic changes on the ECG during typical attacks, or positive non-drug-induced coronary spasm provocation test (e.g. hyperventilation or exercise test), or positive drug-induced coronary spasm provocation test (e.g. acetylcholine or ergonovine provocation test). The patient is considered to have suspected VSA when the ischemic changes on the ECG during attacks are borderline and no clear finding of myocardial ischemia or coronary spasm is obtained in any examination. VSA is considered unlikely if ischemic changes were absent on the ECG or the ECG was not performed during the attack and none of the previous conditions was present. (Adapted from JCS Joint Working Group<a class="elsevierStyleCrossRef" href="#bib0085">4</a>)." ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:13 [ 0 => array:3 [ "identificador" => "bib0070" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Coronary artery spasm as a cause of angina" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:1 [ 0 => "S. 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Case report

A 75-year-old woman with chest pain and transient severe left ventricular systolic dysfunction

Mulher de 75 anos com dor torácica e disfunção sistólica ventricular esquerda grave transitória

Jennifer Mancioa,

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pdccv0104593@med.up.pt

Corresponding author.

, Daniel Caeiroa, Rita Fariaa, Miguel Marquesb, Sofia Bernardinob, Marco Oliveiraa, Aníbal Albuquerquea, Vasco Gama Ribeiroa

a Department of Cardiology, Centro Hospitalar de Vila Nova de Gaia e Espinho, Vila Nova de Gaia, Portugal

b Department of Medicine, Centro Hospitalar do Médio-Ave, Vila Nova de Gaia, Portugal

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obtained approximately six hours after the onset of chest pressure&#44; revealed normal sinus rhythm with widespread ST-segment depression &#40;1&#8211;2 mm in leads V2 to V6&#44; DI and aVl&#44; DII&#8211;III and aVF&#41; &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Figure 1</a>A&#41;&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0025" class="elsevierStylePara elsevierViewall">The electrocardiographic findings were consistent with myocardial ischemia&#44; but other conditions associated with ST-segment depression and mimicking myocardial ischemia also had to be considered&#46; An echocardiogram can help with differential diagnosis by identifying regional wall motion abnormalities&#44; a native or prosthetic valve disorder&#44; pericardial effusion&#44; mechanical complications of acute myocardial infarction &#40;as noted above&#41;&#44; or even proximal aortic disease&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">Transthoracic echocardiography performed in the ER revealed global hypokinesis and impaired left ventricular function with severely depressed ejection fraction &#40;EF&#41;&#59; 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white-cell count 10<span class="elsevierStyleHsp" style=""></span>300&#47;ml&#44; serum creatinine 0&#46;7 mg&#47;dl&#44; blood glucose 106 mg&#47;dl&#44; creatine kinase 135 IU&#47;dl&#44; creatine kinase MB isoenzyme 14&#46;1 ng&#47;ml&#44; and serum troponin I 1&#46;43 ng&#47;ml&#46;</p><p id="par0050" class="elsevierStylePara elsevierViewall">Mildly elevated cardiac biomarkers confirmed myocardial injury but were inconsistent with chest pain six hours after clinical onset&#46; These levels were somewhat unexpected and suggested either spontaneous intermittent coronary reperfusion throughout the day or another cardiovascular condition&#44; such as apical ballooning syndrome&#44; myocarditis or pulmonary embolism&#46;</p><p id="par0055" class="elsevierStylePara elsevierViewall">Preparations were made for transfer to a hospital where percutaneous coronary intervention &#40;PCI&#41; could be carried out&#46; On the patient&#39;s arrival at the PCI-capable hospital&#44; her chest pressure had improved but was not completely resolved&#59; 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it was hypothesized that a thrombus formed on the LAD plaque could have transiently limited coronary blood flow&#46; She was discharged home after six days of hospitalization on medication with aspirin 100 mg once daily&#44; warfarin&#44; atorvastatin 40 mg once daily&#44; bisoprolol 2&#46;5 mg once daily&#44; and transcutaneous nitroglycerin 5 mg 12 hours a day&#46; Cardiac contrast-enhanced magnetic resonance imaging &#40;cMRI&#41; was scheduled for two weeks later which revealed inferoseptal transmural infarct scar&#44; inferior and inferolateral subendocardial infarct and mid-basal ischemia in the anterior and anterolateral walls &#40;<a class="elsevierStyleCrossRef" href="#fig0020">Figure 4</a>&#41;&#46;</p><elsevierMultimedia ident="fig0020"></elsevierMultimedia><p id="par0085" class="elsevierStylePara elsevierViewall">One month after discharge&#44; the patient was readmitted to the cardiac intensive care unit because of recurrent chest pain with hemodynamic instability&#59; her blood pressure was 70&#47;44 mmHg and her heart rate was 125 bpm&#46; 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At baseline coronary angiography showed no new stenosis or coronary blood flow impairment&#59; after ACh injection into the LAD chest pain&#44; ST-segment depression&#44; LAD TIMI blood flow of 1 and transient grade 3 atrioventricular &#40;AV&#41; block were documented&#46; Intracoronary administration of nitrates reversed the coronary spasm and AV conduction disturbances&#46; Twenty minutes later&#44; chest pain and ischemic ST changes recurred&#59; response to nitrate infusion was poor and cardiac arrest with pulseless electrical activity occurred&#46; Advanced life support was maintained for 32 minutes without return of spontaneous circulation&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">Clinical and angiographic diagnosis</span><p id="par0095" class="elsevierStylePara elsevierViewall">Vasospastic angina &#40;left anterior descending coronary artery spasm&#41;&#46;</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0065">Discussion</span><p id="par0100" class="elsevierStylePara elsevierViewall">Coronary artery spasm is one of the important functional abnormalities of the coronary arteries and plays a significant role in the pathogenesis of a wide variety of ischemic heart disease and arrhythmic events&#46; Provocative testing for coronary artery spasm is useful for the diagnosis of vasospastic angina &#40;VSA&#41;&#46; However&#44; these tests are thought to have a potential risk of irreversible ischemia and arrhythmic complications&#46;</p><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0070">Definition and pathology of vasospastic angina</span><p id="par0105" class="elsevierStylePara elsevierViewall">VSA is a condition in which a relatively large coronary artery transiently exhibits abnormal contraction&#46; The initial description of VSA considered vasomotor instability as a key mechanism&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">1</span></a> Prinzmetal et al&#46; described a variant form of angina&#44; which was later confirmed to be coronary spasm&#44; and characterized by symptoms at rest &#40;not during exertion&#41; with ST elevation &#40;not depression&#41; on the ECG&#59; it usually occurs in the early hours of the morning during depressed vagal tone and is associated with occlusion or near occlusion &#40;&#62;90&#37; stenosis&#41; of a focal proximal coronary segment on angiography&#46;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">2</span></a> Currently&#44; it is accepted that both ST-segment elevation and depression can occur&#46; In cases of a coronary artery completely or nearly completely occluded by spasm&#44; transmural ischemia can occur and in turn cause anginal attacks with ST elevation on the ECG&#46; However&#44; if a coronary artery is partially occluded or diffusely narrowed by spasm&#44; or if it is completely occluded by spasm but sufficient collateral flow has developed distally&#44; nontransmural ischemia occurs&#44; causing anginal attacks with ST depression on the ECG&#46;<a class="elsevierStyleCrossRefs" href="#bib0080"><span class="elsevierStyleSup">3&#44;4</span></a></p><p id="par0110" class="elsevierStylePara elsevierViewall">The precise mechanism responsible for coronary spasm remains largely unknown&#59; evidence suggests that the pathogenesis of coronary spasm differs from that of coronary atherosclerosis-based stenosis&#46; Previous studies described different patterns of angiographic changes during the provocation test&#44; including focal and diffuse spasm&#46;<a class="elsevierStyleCrossRefs" href="#bib0080"><span class="elsevierStyleSup">3&#8211;5</span></a> The diffuse spasm pattern is reported to be more common in Japanese than Caucasian patients &#40;20&#37; vs&#46; 7&#37;&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0095"><span class="elsevierStyleSup">6&#44;7</span></a> The focal spasm pattern is more frequently associated with a thicker coronary artery intima-media layer than the diffuse pattern and is induced in a setting of relatively advanced atherosclerotic lesions&#46;<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">8</span></a> Older age&#44; current smoking&#44; high levels of high-sensitivity C-reactive protein&#44; and elevated serum levels of remnant lipoprotein have been also identified as significant risk factors for VSA&#46;<a class="elsevierStyleCrossRefs" href="#bib0110"><span class="elsevierStyleSup">9&#8211;11</span></a></p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0075">Diagnostic criteria</span><p id="par0115" class="elsevierStylePara elsevierViewall">Current guidelines from the European Society of Cardiology<a class="elsevierStyleCrossRef" href="#bib0125"><span class="elsevierStyleSup">12</span></a> and the American Heart Association&#47;American College of Cardiology<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">13</span></a> hardly address the issue of VSA diagnosis and treatment since no large-scale clinical studies of this condition have been performed&#46; The scientific committee of the Japanese Circulation Society &#40;JCS&#41;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">4</span></a> has drawn up guidelines on the diagnosis and treatment of VSA&#46; A flowchart for the diagnosis of VSA proposed by the JCS is illustrated in <a class="elsevierStyleCrossRef" href="#fig0025">Figure 5</a>&#46;</p><elsevierMultimedia ident="fig0025"></elsevierMultimedia><p id="par0120" class="elsevierStylePara elsevierViewall">According to the JCS guidelines&#44; VSA is considered definite if the patient has clearly ischemic changes on the ECG during typical attacks&#44; or a positive non-drug-induced coronary spasm provocation test &#40;e&#46;g&#46; hyperventilation or exercise test&#41;&#44; or a positive drug-induced coronary spasm provocation test &#40;e&#46;g&#46; acetylcholine or ergonovine provocation test&#41;&#46; The patient is considered to have suspected VSA when the ischemic changes on the ECG during attacks are borderline and no clear finding of myocardial ischemia or coronary spasm is obtained in any examination&#46; VSA is considered unlikely if ischemic changes were absent on the ECG or the ECG was not performed during the attack and none of the previous conditions was present&#46;</p><p id="par0125" class="elsevierStylePara elsevierViewall">Pharmacological provocation testing performed during coronary angiography is recommended in patients in whom VSA is suspected based on symptoms&#44; but who have not been diagnosed with coronary spasm by non-invasive evaluation&#46; It is contraindicated in patients considered at high risk of suffering a life-threatening complication of induced coronary spasm &#40;e&#46;g&#46; patients with left main coronary trunk lesions&#44; multivessel disease or untreated congestive heart failure&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">4</span></a></p></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0080">Usefulness and safety of provocative tests</span><p id="par0130" class="elsevierStylePara elsevierViewall">Pharmacological &#40;i&#46;e&#46; ergonovine or ACh&#41; and non-pharmacological &#40;i&#46;e&#46; hyperventilation&#41; provocation tests of coronary spasm during coronary angiography are established as a useful tool for the diagnosis of VSA&#44; because coronary spasm develops transiently and it is not easy to document spontaneous attacks in a clinical context&#46; The first provocation test with ergonovine during coronary angiography was performed at the Cleveland Clinic in 1973&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">1</span></a> Subsequently Specchia et al&#46; and Yasue et al&#46; reported the use of ACh for the induction of coronary spasm&#46;</p><p id="par0135" class="elsevierStylePara elsevierViewall">The intracoronary injection of ACh is known to have high sensitivity &#40;90&#37;&#41; and specificity &#40;99&#37;&#41; for the diagnosis of VSA&#59; however&#44; these tests are thought to have a potential risk of serious complications&#44; including ventricular tachycardia &#40;VT&#41;&#44; ventricular fibrillation &#40;VF&#41;&#44; and bradyarrhythmias&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">1</span></a> Recently&#44; the safety and clinical implications of provocation tests were evaluated in a total of 1244 VSA patients from the nationwide multicenter registry of the Japanese Coronary Spasm Association&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">6</span></a> The provocation tests were performed with either ACh &#40;57&#37;&#41; or ergonovine &#40;40&#37;&#41;&#44; and VT&#47;VF and bradyarrhythmias developed in 3&#46;2&#37; and 2&#46;7&#37;&#44; respectively&#46; Overall&#44; the incidence of arrhythmic complications was 6&#46;8&#37;&#44; a comparable incidence to that during spontaneous angina attack &#40;7&#46;0&#37;&#41;&#46; Multivariate logistic regression analysis demonstrated that diffuse RCA spasm and the use of ACh had a significant correlation with provocation-related VT&#47;VF&#46; Mixed &#40;focal plus diffuse&#41;-type multivessel spasm had an important association with major adverse cardiac events in multivariate Cox proportional hazard regression analysis &#40;adjusted hazard ratio&#44; 2&#46;84&#59; 95&#37; confidence interval 1&#46;34&#8211;6&#46;03&#44; p&#60;0&#46;01&#41;&#44; whereas provocation-related arrhythmias did not&#46; The authors concluded that provocation tests have an acceptable level of safety and usefully information for the risk prediction of VSA patients&#46; A previous study indicated that baseline QT dispersion was significantly greater in VSA patients complicated by ventricular arrhythmias&#46; Slower infusion of provocation agents may reduce the incidence of arrhythmic complications&#44; although excessively slow infusion of ACh may also lead to underestimation of the prevalence of coronary spasm&#46;</p></span></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0085">Conclusions and areas of uncertainty</span><p id="par0140" class="elsevierStylePara elsevierViewall">The use of provocation tests for the detection of abnormal coronary vasomotion in patients with anginal symptoms but angiographically unobstructed coronary arteries not only provides reassurance to the patient that a cause for the symptoms has been found&#44; but also enables the physician to initiate appropriate medical therapy &#40;calcium channel blockers and nitrates&#41; aimed at reducing morbidity and mortality&#46; This may also have important implications for healthcare systems&#44; because most healthcare-related costs in patients with unobstructed coronary arteries are due to recurrent or ongoing angina pectoris&#46; Although rare&#44; the risks of provocation tests are potentially fatal and they should be avoided in patients with left main disease&#44; multivessel disease&#44; severe left ventricular dysfunction&#44; or acute heart failure&#46; Future studies are needed to assess the safety and effectiveness of intracoronary ACh provocation testing in a contemporary cohort of Caucasian patients with unobstructed coronary arteries&#46;</p></span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0090">Ethical disclosures</span><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0095">Protection of human and animal subjects</span><p id="par0145" class="elsevierStylePara elsevierViewall">The authors declare that no experiments were performed on humans or animals for this study&#46;</p></span><span id="sec0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0100">Confidentiality of data</span><p id="par0150" class="elsevierStylePara elsevierViewall">The authors declare that they have followed the protocols of their work center on the publication of patient data&#46;</p></span><span id="sec0055" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0105">Right to privacy and informed consent</span><p id="par0155" class="elsevierStylePara elsevierViewall">The authors have obtained the written informed consent of the patients or subjects mentioned in the article&#46; The corresponding author is in possession of this document&#46;</p></span></span><span id="sec0060" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0110">Funding</span><p id="par0160" class="elsevierStylePara elsevierViewall">This work has no funding&#46;</p></span><span id="sec0065" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0115">Conflicts of interest</span><p id="par0165" class="elsevierStylePara elsevierViewall">The authors have no conflicts of interest to declare&#46;</p></span></span>"
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        "titulo" => "Abstract"
        "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Introduction</span><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Coronary spasm can cause myocardial ischemia and angina in both patients with and without obstructive coronary artery disease&#46; However&#44; provocation tests using intracoronary acetylcholine &#40;ACh&#41; have been rarely performed in the Western world&#46;</p></span> <span id="abst0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0015">Case report</span><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">We report a case of a 75-year-old woman with a history of hypertension and a mechanical aortic prosthesis who presented in the emergency room with acute-onset chest pain&#44; widespread ST-segment depression and severe left ventricular systolic dysfunction&#44; with no signs of prosthesis dysfunction&#46; Emergent coronary angiography excluded obstructive coronary artery disease&#46; Pain relief and normalization of ST segment and systolic function occurred within six hours&#46; The patient was treated for a possible thromboembolic myocardial infarction and was discharged home asymptomatic&#46; Two weeks later&#44; cardiac magnetic resonance was performed showing inferoseptal transmural infarct scar&#44; inferior and inferolateral subendocardial infarct and mid-basal ischemia in the anterior and anterolateral walls&#46; She was readmitted with recurrence of chest pain and it was decided to perform a provocation test with ACh&#46; After injection of ACh into the left anterior descending artery&#44; chest pain&#44; ST-segment depression&#44; blood flow impairment &#40;TIMI 1&#41; and transient grade 3 atrioventricular &#40;AV&#41; block occurred&#46; Intracoronary administration of nitrates reversed the coronary spasm and AV conduction disturbances&#46; Twenty minutes later&#44; chest pain and ischemic ST changes recurred&#59; there was no response to vasodilators and the patient developed cardiac arrest with pulseless electrical activity&#46; Advanced life support was maintained for 32 minutes without return of spontaneous circulation&#46;</p></span> <span id="abst0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0020">Conclusions</span><p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Provocation tests have a high sensitivity and specificity for the diagnosis of vasospastic angina&#46; Although it is rare&#44; these tests have the potential risk of irreversible spasm leading to arrhythmia and death&#46;</p></span>"
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        "resumen" => "<span id="abst0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Introdu&#231;&#227;o</span><p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">O espasmo coron&#225;rio pode causar isquemia mioc&#225;rdica e angina em doentes com e sem doen&#231;a coron&#225;ria obstrutiva&#46; Contudo&#44; os testes de provoca&#231;&#227;o com administra&#231;&#227;o intracoron&#225;ria de acetilcolina &#40;ACh&#41; t&#234;m sido raramente usados no mundo ocidental&#46;</p></span> <span id="abst0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Descri&#231;&#227;o do caso</span><p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">Mulher de 75 anos com hipertens&#227;o arterial e pr&#243;tese mec&#226;nica a&#243;rtica admitida no servi&#231;o de urg&#234;ncia por dor tor&#225;cica aguda&#44; depress&#227;o generalizada do segmento ST e disfun&#231;&#227;o sist&#243;lica grave do ventr&#237;culo esquerdo sem evid&#234;ncia de disfun&#231;&#227;o prot&#233;sica&#46; Realiz&#225;mos angiografia coron&#225;ria emergente que excluiu doen&#231;a coron&#225;ria obstrutiva&#46; Seis horas ap&#243;s admiss&#227;o&#44; a dor&#44; as altera&#231;&#245;es de ST e a disfun&#231;&#227;o ventricular normalizaram&#46; Foi tratado como poss&#237;vel enfarte do mioc&#225;rdio tromboemb&#243;lico e teve alta assintom&#225;tica&#46; Duas semanas ap&#243;s&#44; realiz&#225;mos resson&#226;ncia magn&#233;tica card&#237;aca que mostrou cicatriz de enfarte transmural inferoseptal e de enfarte subendoc&#225;rdico inferior e inferolateral&#44; e isquemia anterior e &#226;ntero-lateral&#46; A doente foi readmitida pela mesma sintomatologia e decidimos realizar estudo de provoca&#231;&#227;o com ACh&#46; Ap&#243;s a inje&#231;&#227;o de ACh na art&#233;ria descendente anterior document&#225;mos dor tor&#225;cica&#44; depress&#227;o do segmento-ST&#44; compromisso do fluxo &#40;TIMI 1&#41; e bloqueio atrioventricular &#40;AV&#41; completo&#46; A administra&#231;&#227;o intracoron&#225;ria de nitratos reverteu o espasmo coron&#225;rio e a perturba&#231;&#227;o da condu&#231;&#227;o AV&#46; No entanto&#44; 20 minutos depois&#44; houve recorr&#234;ncia de dor e altera&#231;&#245;es de ST sem resposta aos vasodilatadores evoluindo a doente para atividade el&#233;trica sem pulso&#46; Mantivemos suporte avan&#231;ado de vida durante 32 minutos sem recupera&#231;&#227;o da circula&#231;&#227;o espont&#226;nea&#46;</p></span> <span id="abst0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Conclus&#227;o</span><p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">Os testes de provoca&#231;&#227;o t&#234;m elevada sensibilidade e especificidade para o diagn&#243;stico de angina vasosp&#225;tica&#46; Apesar de raro&#44; estes testes tamb&#233;m podem levar ao espasmo coron&#225;rio irrevers&#237;vel&#44; arritmia e morte&#46;</p></span>"
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          "en" => "<p id="spar0035" class="elsevierStyleSimplePara elsevierViewall">&#40;A&#8211;C&#41; Electrocardiography&#46; A 12-lead electrocardiogram obtained six hours after onset of chest pressure revealed normal sinus rhythm with widespread ST-segment depression &#40;1&#8211;2 mm in leads V2 to V6&#44; DI and aVl&#44; DII&#8211;III and aVF&#41; &#40;A&#41;&#59; the chest pain and ST-segment depression resolved &#40;B&#41;&#59; the patient was readmitted with recurrence of chest pain and marked ST depression in all precordial leads &#40;C&#41;&#46;</p>"
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          "en" => "<p id="spar0045" class="elsevierStyleSimplePara elsevierViewall">&#40;A&#8211;D&#41; Echocardiography&#46; Transthoracic echocardiogram performed after pain relief showed mean gradient between the aortic and left ventricular systolic pressures of 26 mmHg &#40;A&#41; and slightly impaired left ventricular systolic function with left ventricular ejection fraction of 49&#37; using the three-dimensional Simpson&#39;s method &#40;B&#41;&#59; transesophageal echocardiography allowed better characterization of the mechanical aortic prosthesis&#44; excluding valve dysfunction &#40;C and D&#41;&#46;</p>"
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          "en" => "<p id="spar0055" class="elsevierStyleSimplePara elsevierViewall">Flowchart for the diagnosis of vasospastic angina &#40;VSA&#41;&#46; VSA can be diagnosed when anginal attacks disappear quickly upon administration of nitroglycerin&#44; and at least one of the following reference items is present&#58; &#40;1&#41; attacks appear at rest&#44; particularly between night and early morning&#59; &#40;2&#41; marked diurnal variation is observed in exercise tolerance &#40;in particular&#44; reduction of exercise capacity in the early morning&#41;&#59; &#40;3&#41; attacks are accompanied by ST elevation on the ECG&#59; &#40;4&#41; attacks are induced by hyperventilation &#40;hyperpnea&#41;&#59; &#40;5&#41; attacks are suppressed by calcium channel blockers but not by beta-blockers&#46; VSA is considered definite if the patient has clearly ischemic changes on the ECG during typical attacks&#44; or positive non-drug-induced coronary spasm provocation test &#40;e&#46;g&#46; hyperventilation or exercise test&#41;&#44; or positive drug-induced coronary spasm provocation test &#40;e&#46;g&#46; acetylcholine or ergonovine provocation test&#41;&#46; The patient is considered to have suspected VSA when the ischemic changes on the ECG during attacks are borderline and no clear finding of myocardial ischemia or coronary spasm is obtained in any examination&#46; VSA is considered unlikely if ischemic changes were absent on the ECG or the ECG was not performed during the attack and none of the previous conditions was present&#46; &#40;Adapted from JCS Joint Working Group<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">4</span></a>&#41;&#46;</p>"
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            3 => array:3 [
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              "referencia" => array:1 [
                0 => array:2 [
                  "contribucion" => array:1 [
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                        0 => array:2 [
                          "colaboracion" => "JCS Joint Working Group"
                          "etal" => false
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                  "host" => array:1 [
                    0 => array:1 [
                      "Revista" => array:6 [
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            4 => array:3 [
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                      "autores" => array:1 [
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                      "Revista" => array:6 [
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Article information

ISSN: 21742049
Original language: English

DOI:10.1016/j.repce.2015.10.010

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2024 June	26	27	53
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2023 October	39	13	52
2023 September	19	23	42
2023 August	16	15	31
2023 July	21	10	31
2023 June	23	10	33
2023 May	23	21	44
2023 April	12	4	16
2023 March	17	19	36
2023 February	23	20	43
2023 January	19	9	28
2022 December	32	17	49
2022 November	37	18	55
2022 October	29	16	45
2022 September	27	22	49
2022 August	24	34	58
2022 July	28	27	55
2022 June	25	18	43
2022 May	30	25	55
2022 April	35	29	64
2022 March	28	25	53
2022 February	57	25	82
2022 January	26	19	45
2021 December	17	26	43
2021 November	38	34	72
2021 October	55	45	100
2021 September	12	24	36
2021 August	26	28	54
2021 July	17	25	42
2021 June	18	15	33
2021 May	22	30	52
2021 April	37	38	75
2021 March	45	13	58
2021 February	36	19	55
2021 January	26	13	39
2020 December	20	7	27
2020 November	24	18	42
2020 October	23	12	35
2020 September	45	18	63
2020 August	16	8	24
2020 July	41	14	55
2020 June	30	16	46
2020 May	39	2	41
2020 April	38	9	47
2020 March	32	7	39
2020 February	66	27	93
2020 January	35	5	40
2019 December	28	3	31
2019 November	32	5	37
2019 October	28	11	39
2019 September	22	9	31
2019 August	27	4	31
2019 July	30	8	38
2019 June	25	12	37
2019 May	23	10	33
2019 April	24	18	42
2019 March	83	11	94
2019 February	78	10	88
2019 January	55	7	62
2018 December	24	11	35
2018 November	100	9	109
2018 October	176	11	187
2018 September	53	10	63
2018 August	81	6	87
2018 July	47	4	51
2018 June	75	6	81
2018 May	81	5	86
2018 April	103	5	108
2018 March	64	11	75
2018 February	51	7	58
2018 January	131	5	136
2017 December	148	14	162
2017 November	27	6	33
2017 October	30	16	46
2017 September	21	3	24
2017 August	29	10	39
2017 July	16	9	25
2017 June	23	4	27
2017 May	30	9	39
2017 April	36	1	37
2017 March	37	27	64
2017 February	32	3	35
2017 January	25	2	27
2016 December	40	8	48
2016 November	18	4	22
2016 October	39	6	45
2016 September	18	12	30
2016 August	16	3	19
2016 July	10	3	13
2016 June	14	1	15
2016 May	11	3	14
2016 April	14	5	19
2016 March	18	12	30
2016 February	24	15	39
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2015 December	17	9	26
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