Myocardial infarction and sudden death after sport: acute coronary angiographic findings

Thirteen patients, seven with acute myocardial infarction and six survivors of sudden death after sport, underwent coronary angiography within a mean of 104 min after the onset of symptoms. The admission electrocardiogram showed transmural myocardial ischemia in all patients. The ischemia-related vessel was occluded in all cases of sudden death and in three cases of acute myocardial infarction. Reperfusion was achieved in eight vessels: after intracoronary streptokinase in three, after intracoronary nitroglycerin in three, and mechanically in two. Coronary spasm was demonstrated in three vessels, and coronary thrombi, in four. The coronary lesion was described as either concentric in two or eccentric with irregular borders in eight. There was a high incidence of eccentric lesions consistent with ruptured plaques. The acute coronary angiographic findings of acute myocardial infarction and sudden death after sport are similar. Physical exercise can provoke myocardial infarction and sudden death probably by inducing plaque rupture that can evoke coronary spasm, thrombosis, or both.     

Asynchronous left ventricular wall motion early after coronary thrombosis.

To study regional wall motion early in the development of acute myocardial infarction, left ventriculograms performed in 24 patients before thrombolysis and within 3.5(1.2) (mean (SD] hours of the onset of pain were digitised frame by frame. Isometric and contour plots of regional wall motion were constructed. In 19 patients (seven with anterior descending, eight with right, and four with circumflex disease) thrombosis was demonstrated on an underlying stenosis. In 10 patients the two remaining coronary arteries were normal, and in nine, one or both showed important disease. Mean values of global indices of left ventricular function, including end diastolic volume, ejection fraction, peak ejection and filling rates, and cavity shape changes were all within normal limits, though end systolic volume was significantly raised. Total systolic amplitude of wall motion was normal in the affected area in all but seven patients (four with anterior descending, two with right, and one with circumflex thrombosis). Dyskinesis of more than 2 mm was seen in only three patients, all with thrombosis of the anterior anterior descending coronary artery, and hyperkinesis was present in four. The commonest abnormality of wall motion was hypokinesis during ejection followed by prolonged inward motion during isovolumic relaxation, which was seen in four patients with anterior descending, seven with right, and three with circumflex artery thrombosis. This was preceded by outward motion during isovolumic contraction and delayed inward motion during ejection in eight with right or circumflex thrombosis. Five of six patients without thrombosis had simple hypokinesis or dyskinesis without asynchrony. Disease of other coronary arteries did not affect the pattern of wall motion seen after right or circumflex coronary artery occlusion but it reduced the incidence of delayed inward motion along the free wall after thrombosis of anterior descending artery. Thus early after acute coronary thrombosis asynchronous wall motion is commoner than simple hypokinesis or dyskinesis. Its persistence suggests that in the setting of coronary artery thrombosis in man, residual contractile activity may persist for up to six hours after the onset of symptoms.     

Asynchronous left ventricular wall motion early after coronary thrombosis

To study regional wall motion early in the development of acute myocardial infarction, left ventriculograms performed in 24 patients before thrombolysis and within 3.5(1.2) (mean (SD] hours of the onset of pain were digitised frame by frame. Isometric and contour plots of regional wall motion were constructed. In 19 patients (seven with anterior descending, eight with right, and four with circumflex disease) thrombosis was demonstrated on an underlying stenosis. In 10 patients the two remaining coronary arteries were normal, and in nine, one or both showed important disease. Mean values of global indices of left ventricular function, including end diastolic volume, ejection fraction, peak ejection and filling rates, and cavity shape changes were all within normal limits, though end systolic volume was significantly raised. Total systolic amplitude of wall motion was normal in the affected area in all but seven patients (four with anterior descending, two with right, and one with circumflex thrombosis). Dyskinesis of more than 2 mm was seen in only three patients, all with thrombosis of the anterior anterior descending coronary artery, and hyperkinesis was present in four. The commonest abnormality of wall motion was hypokinesis during ejection followed by prolonged inward motion during isovolumic relaxation, which was seen in four patients with anterior descending, seven with right, and three with circumflex artery thrombosis. This was preceded by outward motion during isovolumic contraction and delayed inward motion during ejection in eight with right or circumflex thrombosis. Five of six patients without thrombosis had simple hypokinesis or dyskinesis without asynchrony. Disease of other coronary arteries did not affect the pattern of wall motion seen after right or circumflex coronary artery occlusion but it reduced the incidence of delayed inward motion along the free wall after thrombosis of anterior descending artery. Thus early after acute coronary thrombosis asynchronous wall motion is commoner than simple hypokinesis or dyskinesis. Its persistence suggests that in the setting of coronary artery thrombosis in man, residual contractile activity may persist for up to six hours after the onset of symptoms.     

Limitation of angiography to identify the culprit plaque in acute myocardial infarction with coronary total occlusion utility of coronary plaque temperature measurement to identify the culprit plaque.

OBJECTIVES: The purpose of this study was to test the hypothesis that the maximal temperature (Tmax) site, as measured by thermal wire, coincides with the culprit plaque by intravascular ultrasound (IVUS) in patients with acute myocardial infarction (AMI). BACKGROUND: Subsequent thrombosis developing to the proximal region from the site of plaque rupture or erosion can potentially complicate the ability of coronary angiography to identify the accurate culprit plaque in patients with coronary total occlusion. METHODS: In 45 consecutive patients with a first anterior AMI, the Tmax site by thermal wire and the culprit plaque by IVUS were evaluated in the left anterior descending coronary artery (LAD). RESULTS: Twenty-five patients had LAD total occlusion, and the remaining 20 had LAD reperfusion. In both groups of patients, the Tmax site was significantly more distal to the angiographically most stenotic site or occlusive site (reperfusion: mean distance [MD] = 1.1 mm distal, 95% confidence interval [CI] 0.3 to 1.9 mm, p = 0.01; total occlusion: MD = 8.8 mm distal, 95% CI 8.0 to 9.6 mm, p < 0.0001). The culprit plaques by IVUS approximately coincided with those by angiography or thermal wire in patients with reperfusion. However, the angiographic occlusive site was significantly more proximal to the culprit plaque by IVUS (MD = 9.2 mm, 95% CI 7.9 to 10.6 mm, p < 0.0001), but the Tmax site coincided with the culprit plaque by IVUS (MD = 0.3 mm distal, 95% CI 0.3 mm proximal to 1.0 mm distal, p = 0.293) in patients with total occlusion. CONCLUSIONS: Temperature measurement of coronary plaque enables accurate localization of the culprit plaque in AMI with coronary total occlusion.     

Coronary artery imaging in the new millennium

Atherosclerotic disease and its thrombotic complications remain the leading causes of mortality and morbidity in Western society. In Australia, cardiovascular disease is responsible for one in every 2.4 (41%) deaths and is the leading single cause of mortality. The crucial final common process for the conversion of a non-occlusive, often clinically silent, atherosclerotic lesion to a potentially fatal condition is plaque disruption. The mortality associated with atherosclerotic disease relates to the acute coronary syndromes, including acute myocardial infarction, unstable angina pectoris and sudden cardiac death. There is substantial clinical, experimental and postmortem evidence demonstrating the role acute thrombosis upon a disrupted atherosclerotic plaque plays in the onset of acute coronary syndromes. Atherosclerotic plaque composition, rather than the stenotic severity, appears to be central in determining risk of both plaque rupture and subsequent thrombogenicity. In particular, a large lipid core and a thin fibrous cap render an atherosclerotic lesion susceptible or vulnerable to these complications. We are currently limited in our ability to accurately identify patients at risk for an acute coronary event. The armamentarium of diagnostic investigations, both non-invasive and invasive, currently clinically available is only able to provide us with data related to the stenotic severity of a coronary artery. The non-invasive testing includes stress-induced (exercise or pharmacological) ischaemic changes in electrical repolarisation, wall motion or myocardial radioactive-tracer uptake. The invasive test of coronary angiography, although the current 'gold standard' for the detection of coronary atherosclerotic disease, provides us with no data about the composition of the atherosclerotic lesion. However, the vast majority of acute coronary events involve a non-critically stenosed atherosclerotic lesion, and thus with currently available means of identification, these lesions would be undetected by stress testing/imaging techniques. Given the critical role that atherosclerotic lesion composition has been shown to play in the risk of both plaque rupture and subsequent thrombogenicity and, consequently, an acute coronary event, new detection techniques need to be investigated for the task of documenting atherosclerotic lesion composition. In the present review we will focus on the status of imaging modalities available for coronary artery imaging and how they may advance our understanding and management of patients with and at risk of coronary artery disease in the new millennium.     

Exercise-induced plaque rupture producing myocardial infarction

A 37-year-old man with unstable angina was subjected to coronary angiography. The right coronary artery showed a minor proximal stenosis, but there were no obstructive lesions in the left coronary artery. He developed a small inferior infarction. He was asymptomatic until re-admission 1 month later, 1 hour after a normal exercise test, with anterior myocardial infarction. Acute coronary angiography showed sub-total occlusion of the left anterior descending artery. The occlusion was partially relieved after intracoronary injection of nitroglycerin. Intracoronary infusion of streptokinase had no further effect. Balloon angioplasty was then successfully performed. It is suggested that stress-induced plaque rupture with intimal hemorrhage and secondary spasm resulted in sub-total occlusion of the left anterior descending artery producing the second myocardial infarction.     

Acute myocardial infarction with normal coronary arteries. In vivo demonstration of coronary thrombosis during the acute episode

Two cases with acute myocardial infarction are presented. Both had thrombotic occlusion of the infarct-related artery. Following successful thrombolysis with streptokinase, coronary angiography was normal. These cases prove that "myocardial infarction with normal coronaries" can be associated with coronary thrombosis in the acute stage.     

Assessment of coronary calcification by electron-beam computed tomography in symptomatic patients with normal, abnormal or equivocal exercise stress test.

AIMS: Exercise stress testing is often used as the initial non-invasive diagnostic test in symptomatic patients with suspected obstructive coronary artery disease. Positive standard ECG criteria are quite specific for obstructive coronary artery disease, but there may be a substantial number of false negative tests, including patients with severe coronary artery disease. Also, exercise stress tests frequently yield equivocal results. Instead of detecting the functional consequences, electron-beam computed tomography visualized atherosclerotic plaque disease directly, but its relationship to functional testing has not been clearly delineated. It was the aim of the current study to examine electron-beam computed tomography for the identification of obstructive coronary artery disease in patients with a normal, abnormal, or equivocal exercise stress test. METHODS AND RESULTS: Symptomatic patients referred for coronary angiography were prospectively included in a consecutive manner if they had no prior diagnosis of coronary artery disease and an unremarkable resting ECG. All patients underwent both exercise stress test and electron-beam computed tomography on the day before coronary angiography. Standard protocols and ECG criteria to diagnose inducible ischaemia were used for the exercise stress test. The electron-beam computed tomography-derived total calcium score was computed according to standard Agatston criteria. Of the 323 patients (mean age, 55+/-11 years; 77% male), 179 (55%) had obstructive coronary artery disease, defined angiographically as luminal diameter narrowing >/=50%. A normal exercise stress test was documented in 105 patients (32.5%), an abnormal exercise stress test ('diagnostic for ischaemia') in 113 (35%), and an equivocal exercise stress test ('inadequate exercise or non-diagnostic ECG-changes') in 105 (32.5%). Multivariate analysis indicated that exercise stress test and electron-beam computed tomography yielded independent information for predicting obstructive coronary artery disease. Sensitivity, specificity and overall accuracy of the exercise stress test were 71%, 75% and 73%, respectively, if equivocal tests were not included, and 50%, 84% and 65% if they were included. Irrespective of the cutpoint regarded as 'positive', the overall accuracy of the electron-beam computed tomography-derived calcium score remained approximately 80% in patients with a normal, abnormal or equivocal exercise stress test. In patients with an equivocal and - to a lesser degree - with a normal exercise stress test, electron-beam computed tomography was able to significantly improve classification regarding obstructive coronary artery disease. Electron-beam computed tomography added no incremental predictive value in patients with an abnormal exercise stress test. CONCLUSION: In patients who are judged to have an intermediate post-test probability of disease after exercise stress test, electron-beam computed tomography scanning may be a meaningful strategy for further stratification regarding the likelihood of obstructive coronary artery disease.     

Arteriographic evidence of coronary arterial spasm in acute myocardial infarction.

Coronary arteriography was performed before and after the intracoronary injection of nitroglycerin to determine the presence or absence of spasm in patients within the first 12 hours of acute myocardial infarction. Coronary arterial spasm was demonstrated in six of fifteen (40%) acute myocardial infarctions associated with coronary artery disease. In five of the six instances the interval from the onset of symptoms to arteriography was less than 6 hours. Spasm was superimposed on a high-grade atherosclerotic obstruction and was separated from the catheter tip by a segment of normal vessel in each instance. The coronary artery remained patent (following the initial relief of spasm) in two patients maintained on sublingual nitrates and heparin. Spasm, superimposed on an atherosclerotic obstruction, may be the primary event or a secondary occurrence in the pathophysiology of acute myocardial infarction. Catecholamines could play an important role in the early pathophysiology of acute myocardial infarction by producing spasm and/or platelet aggregation at the site of an atherosclerotic obstruction. A dynamic interaction between spasm, platelet aggregates and the atherosclerotic plaque may precede coronary thrombosis.     

Successful Management of an Iatrogenic Left Main Coronary Artery Occlusion during Coronary Angiography: A Case Report and Brief Review

Abrupt left main coronary artery (LMCA) closure during diagnostic coronary angiography is a rare but catastrophic event with a poor prognosis. Emergency reperfusion of the LMCA with hemodynamic support should be the primary goal in patients with acute LMCA occlusion. Emergency coronary artery bypass graft surgery may be effective but time-consuming, and carries the risk of extensive and irreversible myocardial damage. We describe a case of abrupt closure of the LMCA due to plaque rupture by a diagnostic angiographic catheter without visible dissection following coronary angiography that was successfully treated with bail-out stenting during cardiopulmonary resuscitation.     

Multiple myocardial infarctions: pancoronary destabilization evaluated by cardiac MRI

PURPOSE: Complete intravascular ultrasound study examination of all three coronary arteries in patients with first acute coronary syndrome very frequently revealed one or more atherosclerotic plaque ruptures associated with the culprit lesion. The aim of this study was to evaluate using cardiac MRI the incidence of multiple necroses in patients with myocardial infarction. The study sought to detect delayed enhancement in a zone different from the necrosis area concerned by the culprit occlusion. METHODS: Eighty consecutive patients who were referred for a first myocardial infarction underwent angioplasty within the first 12hours after chest pain beginning. Each patient was examined within four to eight days following the acute phase. Cardiac MRI evaluated left-ventricle function (TrueFISP sequence) and used a T2 weighted short-inversion-time, inversion recovery sequence (STIR) in order to visualize myocardial oedema; delayed enhancement imaging data were then acquired after injection of gadolinium. RESULTS: In eight patients (10%), we observed two delayed enhancement areas associated with wall-motion abnormalities. One was attributed to the culprit occlusion; the second corresponded to a different coronary artery. In five patients, this second zone was related to an old coronary occlusion confirmed by angiography and the STIR sequence. However, in three patients, the second delayed enhancement area corresponded to a coronary artery stenosis with normal flow. CONCLUSION: In patient with acute myocardial infarction, MRI sometimes detects a necrosis area which was not initially suspected. This observation illustrates the consequences of pancoronary destabilization.     

Acute myocardial infarction complicating primary antiphospholipid syndrome after aspirin and steroids withdrawal

A 24-year-old woman, with known antiphospholid antibodies (APS), presented with an acute myocardial infarction (AMI) that occurred three months after delivery. No risk factors for arteriosclerosis and no past history of arterial/venous thrombosis were noted. During pregnancy, aspirin prophylaxis was prescribed and followed by steroids after caesarian section. Steroids withdrawal was followed by AMI. Immediate coronary angiography revealed thrombotic occlusion of the left descending coronary artery; PTCA was successfully performed. She was discharged with an antiplatelet and anticoagulant regimen. No recurrent coronary event occurred during follow-up.     

A Case of ST Elevation Myocardial Infarction Secondary to Heparin-induced Thrombocytopaenia with Thrombosis

A 54 year-old woman with Noonan Syndrome presented with an acute anterolateral ST elevation myocardial infarction two weeks post septal myectomy and heparin exposure, on the background of known normal coronary arteries. Coronary angiography revealed acute thrombosis of the left main, left anterior descending and left circumflex arteries, which was successfully treated by percutaneous coronary intervention with overlapping bare metal stents. A positive heparin induced platelet antibody test and dramatic fall in platelet count confirmed the diagnosis of heparin induced thrombocytopaenia with thrombosis (HITTS) as the underlying diagnosis. This represents the first documented case of HITTS induced left main coronary artery thrombosis and occlusion.     

Acute myocardial infarction with normal and near normal coronary arteries: Documentation with coronary arteriography within of the onset of symptoms in two cases (three episodes)

Three instances (in two patients) of acute myocardial infarction associated with arteriographically normal or near normal coronary arteries are reported. One patient with a lateral infarction had a normal coronary arteriogram and hypokinesia of the lateral wall. Another patient had two infarctions: (1) a transmural inferior-lateral infarction associated with occlusion of the most distal segment of the posterior descending branch of the right coronary artery, and (2) a transmural anterior-lateral-superior infarction associated with occlusion of the most distal segment of the left anterior descending coronary artery. Neither occlusion was consistent with the extent of infarction. Although coronary arteriography was performed as early as , and , respectively, after the onset of symptoms of infarction in these three instances, the pathophysiologic features of the infarctions are obscure. Temporary occlusion of an epicardial coronary artery by spasm or platelet aggregates, or both, is suggested as a possible mechanism of the acute event.     

Acute myocardial infarction with normal and near normal coronary arteries Documentation with coronary arteriography within 12 1/2hours of the onset of symptoms in two cases (three episodes)

Three instances (in two patients) of acute myocardial infarction associated with arteriographically normal or near normal coronary arteries are reported. One patient with a lateral infarction had a normal coronary arteriogram and hypokinesia of the lateral wall. Another patient had two infarctions: (1) a transmural inferior-lateral infarction associated with occlusion of the most distal segment of the posterior descending branch of the right coronary artery, and (2) a transmural anterior-lateral-superior infarction associated with occlusion of the most distal segment of the left anterior descending coronary artery. Neither occlusion was consistent with the extent of infarction. Although coronary arteriography was performed as early as 12 1/2, 3 3/4 and 11 2/3hours, respectively, after the onset of symptoms of infarction in these three instances, the pathophysiologic features of the infarctions are obscure. Temporary occlusion of an epicardial coronary artery by spasm or platelet aggregates, or both, is suggested as a possible mechanism of the acute event.     

Chronic occlusion of the left main coronary artery: importance of collaterals

Chronic occlusion of the left coronary artery is an infrequent finding in patients undergoing coronary angiography. These patients usually present symptoms of angina or heart failure. We describe a patient who was training regularly without cardiac symptoms until ventricular fibrillation suddenly occurred during a long-distance run. A chronic left main stem occlusion with well-developed right-to-left coronary collaterals was demonstrated by angiography. Up to this event, the collateral flow had been sufficient to allow physical exercise at a high performance level without symptoms. The patient later underwent coronary bypass surgery and recovered completely.     

Detection of coronary artery disease by thallium scintigraphy in patients with valvar heart disease

In patients with valvar heart disease detection of coronary artery disease by conventional non-invasive methods may be difficult. The usefulness of thallium-201 exercise scintigraphy for detecting coronary artery disease was evaluated in 16 patients with aortic stenosis, 17 with aortic regurgitation, nine with mitral stenosis, and six with mitral regurgitation who were investigated by coronary angiography. Only two of 21 patients with greater than or equal to 50% coronary artery obstruction had normal thallium images. Three patients without angiographic evidence of coronary artery stenoses had perfusion defects demonstrated by thallium scintigraphy. Only one patient with greater than or equal to 75% coronary stenosis had a normal thallium scan. Angina pectoris or ST segment depression evoked by exercise test were not useful in distinguishing patients with coronary artery disease from those with normal coronary vessels. These data suggest that thallium exercise scintigraphy may be a useful non-invasive test for detecting coronary artery disease in patients with valvar heart disease.     

Spontaneous coronary artery dissection as a rare cause of an acute coronary syndrome

Spontaneous coronary artery dissection is a rare cause of an acute coronary syndrome. This report describes a previously healthy woman without cardiovascular risk factors who presented with an acute anterior non-ST elevation myocardial infarction. Coronary angiography revealed an isolated longitudinal dissection in the middle part of the left anterior descending coronary artery (LAD) with normal flow of the contrast media. The patient was treated conservatively with heparin, aspirin, clopidogrel, and beta-receptor blocker. Stress exercise test was normal at discharge. After an event-free follow-up of three and a half months coronary angiography showed a completely normal LAD. Literature about epidemiology, pathogenesis, diagnosis and treatment of spontaneous coronary artery dissection is reviewed.     

Detection of coronary artery disease by thallium scintigraphy in patients with valvar heart disease.

In patients with valvar heart disease detection of coronary artery disease by conventional non-invasive methods may be difficult. The usefulness of thallium-201 exercise scintigraphy for detecting coronary artery disease was evaluated in 16 patients with aortic stenosis, 17 with aortic regurgitation, nine with mitral stenosis, and six with mitral regurgitation who were investigated by coronary angiography. Only two of 21 patients with greater than or equal to 50% coronary artery obstruction had normal thallium images. Three patients without angiographic evidence of coronary artery stenoses had perfusion defects demonstrated by thallium scintigraphy. Only one patient with greater than or equal to 75% coronary stenosis had a normal thallium scan. Angina pectoris or ST segment depression evoked by exercise test were not useful in distinguishing patients with coronary artery disease from those with normal coronary vessels. These data suggest that thallium exercise scintigraphy may be a useful non-invasive test for detecting coronary artery disease in patients with valvar heart disease.     

Coronary thrombosis and subsequent lysis after a marathon

A patient who developed an acute anterior myocardial infarction after completion of a marathon is presented. Coronary angiography performed 5 hours after the onset of symptoms showed occlusion of the left anterior descending coronary artery and nonocclusive thrombus in the proximal right coronary artery. Repeat angiography 10 days later showed complete resolution of thrombosis in both arteries. The relation between marathon running and coronary thrombosis is discussed.