Acute ischaemic lesions in death due to ischaemic heart disease. An autopsy study of 333 cases of out-of-hospital death

The frequency of acute coronary artery thrombus and myocardial infarction in subjects dying suddenly or unexpectedly from ischaemic heart disease (IHD) is still unclear, with previous autopsy studies reporting an incidence between 4% and 100%. In this study of 333 randomly selected out-of-hospital deaths, detailed autopsy showed IHD as the sole cause of death in 206 (62%). One hundred and seventeen acute coronary thrombi were present in 96 cases whilst four had an established acute infarct without an identifiable coronary thrombus. Thus 100 (48.5%) IHD deaths had evidence of an acute ischaemic lesion. Acute lesions were equally prevalent among males and females, but the incidence declined with increasing age and they were less frequent among those with a prior clinical history of heart disease. One hundred and forty-seven IHD deaths were witnessed. The proportion of cases with an acute ischaemic lesion increased with the duration of pre-morbid symptoms. Of those with an acute lesion, only 17% died without symptoms compared to 63% of those without an acute lesion. All cases with symptoms lasting more than 3.5 h had an acute lesion. Overall, almost half out-of-hospital IHD deaths in this study were related to an acute ischaemic lesion. Differences in the detail of the pathological examination and examination of differing sub-groups of the out-of-hospital death population probably account for the differing results of previous studies.     

Pathogenesis of acute coronary syndromes

Coronary artery diseases may categorized into asymptomatic disease, angina pectoris, myocardial infarction, chronic heart failure, and sudden coronary death. Unstable angina, acute myocardial infarction, and sudden cardiac death are known as the acute coronary syndromes. Coronary atheroma is unstable in the patients with acute coronary syndromes. Stable plaques will be unstable when dynamic alterations occur. The alterations are plaque rupture, plaque hemorrhage, coronary thrombosis and vasospasm. They act each other. We analysed the histopathology of coronary arteries who died of acute myocardial infarction in 85 cases. It showed that the risk factors of plaque rupture are clusters of form cells, eccentric plaque with soft lipid rich core, and thinning of fibrous cap in atheroma. Most of these cases ruptured at edge of the atheroma.     

Intravascular ultrasound assessment of direct percutaneous transluminal coronary angioplasty in patients with acute myocardial infarction

BACKGROUND: Acute myocardial infarction is caused by sudden thrombotic occlusion of the coronary artery due to a previous rupture of atherosclerotic plaque. OBJECTIVE: To use intracoronary ultrasound measurements to evaluate lumen and plaque changes in patients with acute myocardial infarction. METHODS: Patients (n = 103) with acute myocardial infarction who had been scheduled to undergo primary percutaneous transluminal coronary angioplasty (PTCA) were selected. Both before and after successful coronary angioplasty, intracoronary 30 MHz ultrasound studies were performed using a 3.5F monorail catheter. The ultrasound catheter was successfully advanced into the occluded vessel segment without major complications prior to PTCA in 79 of 103 (76.7%) patients and after PTCA in 88 of 103 (85.3%) patients. RESULTS: The plaques were eccentric in 66 patients (83.5%). The plaque morphology was purely low echogenic in 14 (17.7%), highly echogenic in six (7.6%) and mixed in 59 (74.7%) patients. Partial (59 of 79, 74.7%) or ring-like calcification (3 of 79, 3.8%) was observed in 62 patients (78.5%). Plaque fissuring or dissection was detected prior to PTCA in 25 patients (31.7%). Coronary angioplasty successfully enlarged the inner luminal area from 2.1 +/- 0.7 to 7.4 +/- 1.9 mm2 (P < 0.01), whereas the plaque-thrombus area decreased significantly (13.8 +/- 1.7 mm2 before and 9.0 +/- 1.9 mm2 after PTCA; P < 0.01). The total vessel area remained virtually constant (15.9 +/- 1.9 mm2 before and 16.4 +/- 2.5 mm2 after PTCA, NS). PTCA-induced plaque rupture or dissection was observed in only 13 (16.5%) patients. CONCLUSION: Intracoronary ultrasound imaging can be performed safely and successfully prior and subsequent to PTCA in selected patients with acute myocardial infarction. Early reperfusion via PTCA seems to be attributable to a significant reduction in the amount of low-echogenic plaque and thrombus material, whereas factors like balloon-induced dissection and stretching of vessels play only a minor role.     

Peri-infarct angiographic behavior of "non-culprit" coronary infarct lesions]

Because systemic factors, such as lipoproteins, autoantigens, infectious agents, may facilitate plaque rupture, thrombus formation and coronary occlusion, the question may arise of whether thrombosis be only a local plaque event or the consequence of an acute activity of the entire coronary tree. Taking changes at the narrowest point of non culprit lesions as reflecting progression or regression of the disease when > 0.27 mm, early (within a few days) and late (within 1 month) coronarographic findings in 23 patients with first infarction were compared with those of patients with stable angina, in whom coronary angiography was performed for diagnostic purposes and was repeated 1 month later, before angioplasty. Sixteen infarction patients had progression, 4 had regression, 1 had both, and 2 had steadiness; corresponding values in stable angina group were 2 (p < 0.001), 1 (NS), 0 (NS) and 20 (p < 0.001). In the infarction group, 17 out of the 45 non culprit lesions progressed and 5 regressed; corresponding figures in stable angina group were 2 (p < 0.001) and 1 (p < 0.05). Three of the infarction patients developed interim angina at rest that was associated with progression of a culprit lesion in each of them. These results support the hypothesis that in a number of cases infarction may not reflect an arbitrary plaque event but rather a systemic coronary disease activity with maximal expression at the level of the offending plaque.     

Unstable atherosclerotic plaque and acute coronary syndromes

Acute coronary syndromes (unstable angina pectoris, acute myocardial infarction, sudden cardiac death) participate significantly in cardiovascular and general morbidities and mortalities. Their common pathogenetic mechanism resides in the disturbance of the integrity of atherosclerotic plaque by a fissure, rupture, or ulceration and the origin of unstable atherosclerotic plaque by the formation of thrombi, which together with vasoconstriction, causes a varying degree of the dynamic obstruction of the coronary artery. Thrombogenesis takes place in coincidence with the factors of vascular wall, rheologic, thrombotic (proaggregatory and procoagulatory), and antithrombotic (antiaggregatory and anticoagulatory-fibrinolytic) factors. The formation of unstable atherosclerotic plaque is a critical point of the dissociation of both stable and unstable myocardial ischaemiae. The prevention and therapy of atherosclerosis must be complex, namely antiatherogenic, however most of all endothelium-protective, or cellulo-protective, antilipidogenic and antithrombogenic. They cannot be alternative; one therapy will not substitute another. Regarding the importance of even residual thrombosis and thrombin, new antithrombotic substances are being intensively investigated.     

Directional coronary atherectomy for the treatment of Palmaz-Schatz in-stent restenosis

Management of in-stent restenosis has become a significant challenge in interventional cardiology. The results of balloon angioplasty have been disappointing due to the high recurrence of restenosis at follow-up. Debulking of the restenotic tissue within the stents using directional coronary atherectomy (DCA) may offer a therapeutic advantage. We report the immediate clinical and angiographic outcomes and long-term clinical follow-up results of 45 patients (46 lesions), mean age 63+/-12 years, 73% men, with a mean reference diameter of 2.9+/-0.6 mm, treated with DCA for symptomatic Palmaz-Schatz in-stent restenosis. DCA was performed successfully in all 46 lesions and resulted in a postprocedural minimal luminal diameter of 2.7+/-0.7 mm and a residual diameter stenosis of 17+/-10%. There were no in-hospital deaths, Q-wave myocardial infarctions, or emergency coronary artery bypass surgeries. Four patients (9%) suffered a non-Q-wave myocardial infarction. Target lesion revascularization was 28.3% at a mean follow-up of 10+/-4.6 months. Kaplan-Meier event-free survival (freedom from death, myocardial infarction, and repeat target lesion revascularization) was 71.2% and 64.7% at 6 and 12 months after DCA, respectively. Thus, DCA is safe and efficacious for the treatment of Palmaz-Schatz in-stent restenosis. It results in a large postprocedural minimal luminal diameter and a low rate of both target lesion revascularization and combined major clinical events at follow-up.     

Myocardial and coronary lesions in anterior and posterior myocardial infarction. Comparative macroscopic anatomical study

Comparative anatomical macroscopic study of two groups of 24 cases of recently fatal first myocardial infarction (anterior or inferior) confirmed certain classical notions: higher age in females (p less than 0.02), inferior necrosis less extensive (p less than 0.05), higher occurrence of rupture of the myocardium in the case or an anterior lesion, and less frequent rupture but more often involving the septum in the case of inferior infarction. Furthermore the study showed the virtually constant presence of an intracoronary thrombus responsible for the infarction, the wider extent of atherosclerotic lesions in the right coronary system, and, above all, a fairly direct opposition between stenotic lesions most often proximal, and affecting the single anterior trunk (75%), in the case of anterior infarction, whilst significant atherosclerotic occlusion of the anterior (87%) and left (67%) systems were seen in the case of inferior infarction due to complete occlusion of the right coronary artery. These anatomical findings indicate the need for routine coronary arteriography after inferior infarctions, the recurrence of chest pain being related not to changes "in sity" but rather to significant occlusion of another coronary system.     

Sudden unexpected death resulting from an anomalous hypoplastic left coronary artery

We present a case of sudden death in a 24-year-old, healthy white female who was physically active and participated in sports, including soccer. Two weeks prior to her death, an insurance physical examination revealed an abnormal electrocardiogram which demonstrated flipped T waves in the anterior leads. There was no other remarkable medical history. At autopsy, only one coronary ostium was demonstrated and it originated from the right aortic sinus. Approximately 0.8 cm from this right coronary artery (RCA) ostium, a left coronary artery (LCA) branched off the RCA at a 90-degree angle. The LCA had luminal diameter of 0.4 m but the LCA had a luminal diameter of only 0.1 cm. The LCA coursed anterior to the base of the pulmonary artery and down the anterior ventricular septum reflecting the usual course of the left anterior descending (LAD) coronary artery. The LCA and RCA paths appeared to merge or terminate at the anterior left ventricular myocardium which was discolored gray, a process that involved the inner and middle thirds of the myocardium. Based on the autopsy findings, we certified the cause of death as a probable arrhythmia due to myocardial fibrosis and dystrophic calcification resulting from complications of an anomalous hypoplastic left coronary artery. Anomalies of coronary arteries have been classified and studied at autopsy and by clinical angiography. Coronary artery anomalies can be divided into minor and major forms with major anomalies often resulting in cardiac dysfunction that may cause failure and death. Minor anomalies, in general, have no pathophysiological significance and are compatible with life. Minor anomalies include variations in number and location of coronary ostia. A single coronary ostia is exceedingly rare in hearts with no other congenital malformations. The prognostic significance can be unpredictable. A single coronary artery has the potential to be dangerous if obstructed at its main stem, or if it branches at an acute angle. Additionally, hypoplasia of one or more coronary arteries has been found to be associated with sudden death.     

Treatment of ostial lesions of the left anterior descending coronary artery with Palmaz-Schatz coronary stent

We evaluated acute and long-term clinical and angiographic results of elective Palmaz-Schatz coronary stent implantation for left anterior descending coronary artery (LAD) ostial stenosis in 23 consecutive patients. Eight patients had stable angina, 14 had unstable angina, and 1 had recent myocardial infarction. Sixteen patients had single-vessel, 5 had double-vessel, and 2 had triple-vessel disease. Clinical success without major complications (death, acute myocardial infarction, emergency coronary artery bypass grafting) was obtained in all cases and technical success in 20 cases (86.9%). After stenting, minimal lumen diameter increased from 1.05 +/- 0.45 mm to 2.89 +/- 0.52 mm (p < 0.001), and percent diameter stenosis decreased from 65.49% +/- 13.36% to 2.94% +/- 19.93% (p < 0.001). One case of subacute thrombosis and no major bleeding occurred. Twenty patients were followed-up for 6 months, during which no acute cardiac event (death, acute myocardial infarction) was observed. Eighteen patients were eligible for follow-up coronary angiography; restenosis (> or = 50% diameter stenosis) was observed in 4 (22.2%). Minimal lumen diameter was 1.77 +/- 0.55 mm, percent diameter stenosis was 39.66% +/- 17.62%, late loss was 1.01 +/- 0.69 mm, net gain was 0.79 +/- 0.55 mm, and loss index (late loss/acute gain) was 0.53 +/- 0.37. This study suggests that elective Palmaz-Schatz stent implantation may be a safe and successful treatment of LAD ostial lesions and provides a large increase in lumen diameter.     

Thrombosis in ischemic heart disease

Thrombus formation on a fissured or disrupted atherosclerotic plaque is the main pathogenetic mechanism for the acute coronary syndromes of myocardial infarction and unstable angina. Myocardial infarction results from an acute total occlusion of the artery, while unstable angina is secondary in most cases to mural thrombus formation. Thrombus formation has also been implicated in chronic atherosclerotic disease progression and in restenosis following coronary angioplasty. Therapeutic measures to treat thrombus rely on the ability of drugs to either prevent thrombus extension, dissolve its fibrin component, or prevent further platelet aggregation. Other measures rely on the ability of intracoronary techniques to open coronary arteries. The primary prevention of intracoronary thrombus formation is evolving. Measures to stabilize plaques or to reduce hypercoagulability are being tested or have been tested in recent trials.     

Angioscopic predictors of early adverse outcome after coronary angioplasty in patients with unstable angina and non-Q-wave myocardial infarction

BACKGROUND: Clinical and angiographic criteria have a limited ability to predict adverse outcome in patients with unstable angina who are undergoing percutaneous transluminal coronary angioplasty (PTCA). We investigated whether the use of angioscopy can improve prediction of early adverse outcome after PTCA. METHODS AND RESULTS: Angioscopic characterization of the culprit lesion was performed before PTCA in 32 patients with unstable angina and 10 with non-Q-wave infarction. Seven patients (17%) had an adverse outcome (myocardial infarction, repeat PTCA, or need for coronary artery bypass graft surgery) within 24 hours after PTCA. Six of 18 patients with a yellow culprit lesion had an adverse outcome compared with 1 of 24 in whom the culprit lesion was white (P = .03). Six of 20 patients with plaque disruption suffered an adverse outcome compared with 1 of 22 with nondisrupted plaques (P = .04). Six of 17 patients with intraluminal thrombus had an adverse outcome, whereas only 1 of 25 patients without thrombus suffered an adverse outcome (P = .01). Yellow color, disruption, and thrombus at the culprit lesion site were associated with an eightfold increase in risk of adverse outcome after PTCA. The prediction of PTCA outcome based on characteristics of the plaque that were identifiable by angioscopy was superior to that estimated by the use of angiographic variables. CONCLUSIONS: In patients with unstable angina and non-Q-wave infarction, angioscopic features of disruption, yellow color, or thrombus at the culprit lesion site can identify patients at high risk of early adverse outcome after PTCA. Angioscopy was superior to angiography for prediction of PTCA outcome.     

Coronary angioscopy: initial experience during coronary interventions

BACKGROUND AND OBJECTIVE: Percutaneous coronary angioscopy (CAG) provides in vivo visual information about the luminal aspect of the vessel. In this report we describe our initial experience with CAG during coronary angioplasty (PTCA). METHODS: Fifty-five patients (age 60 +/- 9 years), 8 female, were included. Most patients, 42 (76%) were treated for unstable angina. RESULTS: In 49 patients (89%) CAG was performed prior to PTCA, and in all cases the intraluminal material responsible of the stenosis was recognized. This included plaque associated to thrombus in 29 patients (59%), isolated plaque in 15 (31%) and isolated thrombus in 5 (10%). Of these plaques, 25 (57%) were yellow, 14 (32%) were yellow and white and 5 (11%) were white. Of the 34 thrombi, 23 (68%) were mural and 11 (32%) protruding. CAG post-PTCA was performed in 43 patients (78%). CAG visualized residual plaque in 41 patients (95%) and residual thrombus in 34 (79%). In addition, CAG recognized dissections in 30 patients (70%). CAG was more sensitive than angiography for the detection of thrombus (pre-PTCA 34 [69%] vs 11 [22%]; p < 0.05, and post-PTCA 34 [79%] vs 5 [12%]; p < 0.05]) and coronary dissections (post-PTCA 30 [70%] vs 19 [44%]; p < 0.05). CAG before intervention caused angina in 39 patients (80%), ventricular fibrillation (successfully managed with DC cardioversion) in 1, and AV block in another patient. The angiographic result deteriorated in 4 patients (9%) immediately after the CAG performed following PTCA. A repeat balloon PTCA was required in these patients. CONCLUSIONS: CAG provides unique information on coronary lumen surface that complements angiographic data. As compared with angiography, CAG is more sensitive in the detection of intracoronary thrombi and dissections. Further studies are required to determine whether the additional information provided by CAG may be used, to select coronary interventions according to specific lesion characteristics, to optimize dilation results and, eventually, to improve the clinical outcome of these patients.     

Multicenter investigation of coronary stenting to treat acute or threatened closure after percutaneous transluminal coronary angioplasty: clinical and angiographic outcomes

OBJECTIVES: This study reports on the initial experience with the Gianturco-Roubin flexible coronary stent. The immediate and 6-month efficacy of the device and the incidence of the complications of death, myocardial infarction, emergency coronary artery bypass surgery and recurrent ischemic events are presented. BACKGROUND: Abrupt or threatened vessel closure after coronary angioplasty is associated with increased risk of myocardial infarction, emergency coronary artery bypass graft surgery and in-hospital death. When dissection or prolapse of dilated plaque into the lumen is unresponsive to additional or prolonged balloon catheter inflation, coronary stenting offers a nonsurgical mechanical means to rapidly restore stable vessel geometry and adequate coronary blood flow. METHODS: From September 1988 through June 1991, 518 patients underwent attempted coronary stenting with the 20-mm long Gianturco-Roubin coronary stent for acute or threatened vessel closure after angioplasty. In 494 patients, one or more stents were deployed. Thirty-two percent of patients received stents for acute closure and 69% for threatened closure. RESULTS: Successful deployment was achieved in 95.4% of patients. Overall, stenting resulted in an immediate angiographic improvement in the diameter stenosis from 63 +/- 25% before stenting to 15 +/- 14% after stenting. Emergency coronary artery bypass graft surgery was required in 4.3% (21 of 493 patients). The incidence of in-hospital myocardial infarction (Q wave and non-Q wave) was 5.5% (27 of 493 patients). At 6 months, myocardial infarction was infrequent, occurring in 1.6% (8 of 493 patients). The incidence of in-hospital death was 2.2% (11 of 493 patients). Late death occurred in 7 patients (1.4%) and 34 patients (6.9%) required later bypass graft surgery. Complications included blood loss, primarily from the arterial access site, and subacute thrombosis of the stented vessel in 43 patients (8.7%). CONCLUSIONS: The early multicenter experience suggests that this stent is a useful adjunct to coronary angioplasty to prevent or minimize complications associated with flow-limiting coronary artery dissections previously correctable only by surgery. Although this study was not randomized, it demonstrated a high technical success rate and encouraging results with respect to the low incidence of emergency coronary artery bypass graft surgery and myocardial infarction.     

Effect of coronary thrombus age on fibrinogen uptake

A study was carried out to define the time limits during which an experimental coronary thrombus remains capable of incorporating fibrinogen. 131I-fibrinogen was given to intact anesthetized dogs at different time intervals, up to 67 hours, following the formation of a coronary thrombus by catheter-electrode. Radioactivity of the recovered thrombi as a whole and segmentally divided, was determined following variable time intervals of exposure to circulating fibrinogen and was expressed as thrombus/blood ratio. The results indicate that coronary thrombi formed in a normal coronary vessel remain capable of incorporating fibrinogen for at least eighteen hours, with no significant differences in the segmental distribution of radioactivity. These findings do not support the view that the recovery of isotopic fibrinogen, which was given after the onset of coronary symptoms, in thrombi from patients with myocardial infarction establishes that the thrombus was initiated after the ischemic process.     

A clinical and pathological study of 46 cases of sudden and unexpected death

A series of 46 autopsied adult cases of sudden and unexpected natural death were investigated. In this study, sudden and unexpected death was defined as any death occurring with 24 hours of onset of symptoms in a person with or without probable cause of death suggested by medical history. The cases included 31 males and 15 females aged 26 to 85 years (mean 66.6 years). Age distribution peaked in seventies. The lesions causing sudden and unexpected death according to the most frequent organ systems were, diseases of the heart (acute myocardial infarction with or without old infarct, 20; old myocardial infarction without acute infarction, 2; dilated cardiomyopathy, 2; sarcoidosis, 1; amyloidosis, 2; and valvular disease, 2), the aorta (ruptured aneurysm, 6; dissecting aneurysm, 2), the respiratory tract (pulmonary embolism, 7; pulmonary hypertension, 1), the alimentary tract (intestinal obstruction, 1), and other diseases (cause unknown, 1). The cardiovascular lesions were found in 78.2% of cases autopsied. The sudden and unexpected death caused by acute myocardial infarction was found in 47.8%, and acute myocardial infarction seemed to play a major role in cardiac sudden death in these series. The respiratory lesions were found in 17.4%. Four of seven cases with pulmonary embolism died in two weeks after surgical operation. The most common underlying disease was post-operative condition.     

The use of relational databases in the transition from quality assurance to continuous quality improvement: a clinical practice model

BACKGROUND AND OBJECTIVE: The solid-state, mid-infrared holmium:YAG laser (2.1 microm wavelength) is a relatively new percutaneous device that has recently been evaluated in a multicenter study. Because of its unique wavelength and photoacoustic effects on atherosclerotic plaques, this laser may be useful in treatment of symptomatic patients with coronary artery disease. This study sought to evaluate the safety and efficacy of mid-infrared laser angioplasty in the treatment of coronary artery lesions. PATIENTS AND METHODS: Laser angioplasty was performed on 2,038 atherosclerotic lesions in 1,862 consecutive patients with a mean age of 61 +/- 11 years. Clinical indications included unstable angina (69%), stable angina (20%), acute infarction (6%), and positive exercise test (5%). Complex lesion morphology included eccentricity (62%), thrombus (30%), total occlusion (27%), long lesions (14%), and saphenous vein grafts (11%). RESULTS: This laser catheter alone successfully reduced stenosis (>20%) in 87% of lesions. With adjunct balloon angioplasty, 93% procedural success was achieved. The presence of thrombus within the target lesion was a predictor of procedural success (OR = 2.0 [95% confidence interval 2.0, 4.0], P = .04). Bifurcation lesions (OR = 0.5 [95% confidence interval 0.2, 1.0], P = .05) and severe tortuosity of the treated vessel (OR = 0.4 [95% confidence interval 0.2, 0.9], P = .02) were identified as significant predictors of decreased laser success. Calcium within the lesion was associated with reduced procedural success (OR = 0.57 [95% confidence interval 0.34, 0.97], P = .03), and calcified lesions required significantly more energy pulses than noncalcified lesions (119 +/- 91 pulses vs. 101 +/- 86 pulses, respectively, P = .0002). Complications included in-hospital bypass surgery 2.5%, Q-wave myocardial infarction 1.2%, and death 0.8%. Perforation occurred in 2.2% of patients; major dissection in 5.8% of patients, and spasm in 12% of patients. No predictor of major complications was identified. Six-month angiographic restenosis was documented in 54% of patients, and clinical restenosis occurred in 34% of patients. CONCLUSION: Mid-infrared laser has a safety profile similar to that of other debulking devices. This laser may be useful in select patients presenting with acute ischemic syndromes associated with intracoronary thrombus; however, like other coronary lasers, it is limited by the need for adjunctive balloon angioplasty and/or stenting to achieve adequate final luminal diameter. No beneficial effects on reducing 6-month restenosis rates were observed.     

Complications prior to revascularization among patients waiting for coronary artery bypass grafting and percutaneous transluminal coronary angioplasty

AIM: To describe the occurrence of death, development of acute myocardial infarction and need for hospitalization among patients on the waiting list for coronary artery bypass grafting and percutaneous transluminal coronary angioplasty. PATIENTS AND METHODS: All the patients on the waiting list for possible coronary revascularization in September 1990 in western Sweden. RESULTS: Of 718 patients waiting for either coronary artery bypass grafting or percutaneous transluminal coronary angioplasty, 15 (2.1%) died between the actual week in September 1990 and prior to revascularization and 12 (1.7%) developed a non-fatal acute myocardial infarction during the same period. All 15 patients who died before undergoing revascularization died a cardiac death. Death and/or the development of an acute myocardial infarction was significantly more frequent among the elderly, among patients with a low ejection fraction and among patients with a history of diabetes mellitus. In all, 29% required hospitalization prior to the procedure. The most common reason was symptoms of angina pectoris requiring hospitalization in 23% of the patients. CONCLUSION: Among patients on the waiting list before either coronary artery bypass grafting or percutaneous transluminal coronary angioplasty, 15 (2.1%) died prior to the procedure and 1.7% developed a non-fatal acute myocardial infarction. The risk of either death or developing an acute myocardial infarction was highest among patients in the older age groups, among patients with a history of diabetes mellitus and among patients with a lower ejection fraction.     

Intramural coronary artery dysplasia of the ventricular septum and sudden death

We report four cases of sudden unexpected death in three males and one female aged 12 to 31 years. Death occurred during exercise in three of four cases, and there was no history of sudden death or previous cardiac history in any patient. At autopsy, there was marked intramural coronary artery dysplasia of the ventricular septum, accompanied in three of the four cases by myocardial fibrosis. The arterial dysplasia was characterized by severe medial thickening with smooth muscle cell disorganization and marked luminal narrowing. There was no evidence of myofiber disarray or asymmetric septal hypertrophy to suggest hypertrophic cardiomyopathy. Other than an ostium secundum type atrial septal defect in one case, there were no associated cardiac or extracardiac lesions found at complete autopsy of these individuals. We conclude that small vessel disease of intramural coronary arteries of the ventricular septum may be an isolated finding leading to sudden cardiac death in young adults.     

The acute coronary ischemic syndromes--the central role of thrombosis

The postulate that thrombotic coronary occlusion was the underlying pathophysiologic event in the acute coronary ischemic syndromes was developed over the years 1912-60. This concept prompted the development of anticoagulant and thrombolytic therapies and the use of acetylsalicylic acid in such patients. A central role for coronary thrombus came to be questioned in the 1970s and the use of anticoagulants dramatically decreased and thrombolytic therapy was little used. Coronary angiographic studies among patients during the early hours of evolving myocardial infarction re-established the etiologic role of coronary thrombosis in the acute coronary ischemic syndromes, and were supplemented by careful autopsy studies. The concepts of meta-analysis lead to more accurate interpretations of earlier randomized, controlled trials of anticoagulant, antiplatelet and thrombolytic therapies. Large clinical trials have provided confirmatory evidence and have established the benefits of antiplatelet and thrombolytic agents in the acute ischemic syndromes. The benefit of long term anticoagulation following myocardial infarction has been demonstrated, although the benefit during the acute in-hospital phase of myocardial infarction is still uncertain. Currently, clinical trials are evaluating new antithrombins, antiplatelet agents, and thrombolytic agents and regimens among patients with unstable angina, acute myocardial infarction, and undergoing angioplasty for complex coronary lesions.     

Ultrasound coronary angioplasty: state of the art and new clinical aspects

Therapeutic ultrasound was shown to ablate thrombi and to disrupt atherosclerotic plaques in vitro and recently to recanalize occluded coronary arteries in acute myocardial infarction (AMI). The goal of this article is to update collective experience and to weigh the promising and unresolved aspects of this newly developed technology and its clinical results. As therapeutic ultrasound was for long known a synonym for lithotripsy of calculi diseases, it lastly received high attention as a catheter-based ultrasound method to ablate thrombi and disrupt atherosclerotic plaques in interventional cardiology (Figure 1). The effect of therapeutic ultrasound to ablate selectively pathological tissue depends on its bioselectivity for elastic fibers: After ultrasound sonication, healthy tissue-rich in elastin and collagen-including arterial wall remains intact whereas thrombus and plaque with their minimal elastic support are found to be highly susceptible to ablation. Our catheter for coronary ultrasound thrombolysis (Figure 2) consists of a solid metal probe and is connected to a piezo-electric transducer at its proximal end. The distal part ends in a three-wire flexible segment with a 1.6 mm tip ball to guarantee maximal wire flexibility and optimal transmission of ultrasound energy. The initial in vitro studies resulted in a fundamental understanding of the destructive effect of ultrasound on tissue based on 4 factors: mechanical vibration, thermal effects, microcurrents, and cavitation. The first studies on human peripheral vessels were published in 1991 being performed during femoral bypass surgery on occluded and partially obstructed arteries. The procedure was performed without perforation, no adverse side effects emerged, restenosis rate was 20%. The clinical application of coronary ultrasound angioplasty was initiated in 1991; Siegel published his data on 44 patients. In his study, 30 patients with chronic atherosclerotic occlusive lesions and 14 with unstable or stable angina or AMI were treated by ultrasound angioplasty. Residual stenosis after ultrasound treatment was 71%, after balloon dilation reduced to 34%. In the 6-month follow-up angiograms showed no major adverse effect or restenosis. Our experience with coronary ultrasound thrombolysis (CUT) is based on the analysis of 33 patients' data in the feasibility (Table 1) plus multicenter phase of the ACUTE trial (Analysis of Coronary Ultrasound Thrombolysis Endpoints) (Figure 3). Our patients were exclusively treated for AMI by ultrasound angioplasty and afterwards by PTCA if required (Figure 4). The average final percent stenosis was 20% (Figure 5). The main efficacy parameters, device success and angiographic success rates were 100%, clinical success rate was 91.7% (Figure 6 and Table 2). The adverse clinical events of CUT are limited--at least in our studies--to reocclusion of infarct-related artery and ischemia and could be reversed by additional PTCA. No adverse clinical side effects were observed during sonication of the coronary tree. Final angiography revealed residual stenosis of 20% without morphological signs. These excellent results suggest that bioselectivity of ultrasound together with the developed skills of the catheter system induces rapid and selective thrombolysis with no need to cross the target lesion before sonication. But what is the better solution for thrombosis and which for plaque disruption? The development of transluminal balloon catheter really modified therapeutic approach to obstructive coronary and peripheral arterial disease but it is still accompanied by a high rate of abrupt closure, AMI and death. Although the use of intravenous thrombolytic agents is well established in the treatment of AMI and these agents are widely used, a large patient collective remains (up to 33% and more) in whom their use is inadvisable due to recent stroke, surgery, trauma or other contraindications. (ABSTRACT TRUNCATED)