Heart rupture as an acute complication of cocaine abuse: A case report.

The purpose of this study is to show a very rare complication of acute cocaine poisoning, namely heart rupture. In the present case report, acute cocaine intoxication caused massive myocardial infarction, resulting in heart rupture and cardiac tamponade. A crime scene investigation found a dead body on the street in a drug dealing district. Examination of the body showed no external injuries. A thorough autopsy was performed showing massive cardiac tamponade with 510 ml of blood within the pericardium and full-thickness tissue lesion at the posterior wall of the left ventricle of 3.5 × 3 cm. Histological examination in hematoxylin and eosin was performed and confirmed the interruption of the posterior wall of the left ventricle with the presence of blood. In fact, although the correlation between cocaine and myocardial damage is well established, the relationship between heart rupture and acute cocaine intoxication is an extremely rare event. Moreover, since there are, to date, few reports of similar deaths, our report provides useful information regarding sudden death in a cocaine abuser. It is, therefore, of crucial importance to report this case to the scientific community.

Cardiac rupture after intravenous t-PA administration in acute ischemic stroke.

BACKGROUND: Ventricular free wall rupture is a fatal complication of myocardial infarction (MI). Although described in MI patients who receive thrombolytic therapy, this complication is not well known in ischemic stroke patients who receive intravenous (IV) t-PA. METHODS: Case report. RESULTS: We present a 93-year-old woman with an acute onset of a right middle cerebral artery syndrome in the setting of subacute MI. IV t-PA was administered and she subsequently developed asystolic arrest and died. Autopsy showed subacute MI, hemopericardium, and rupture of the left ventricle. CONCLUSIONS: This case illustrates a fatal cardiac complication of IV thrombolytic therapy for stroke. The speculated mechanism is hemorrhage into the infarcted myocardium.

Fatal amphetamine-associated cardiotoxicity and its medicolegal implications.

Amphetamines are popular drugs of abuse, particularly among youngsters and at dance scenes. Cardiotoxicity (manifested as cardiomyopathy, acute myocardial infarction/necrosis, heart failure, or arrhythmia) after the recreational (mis)use of amphetamine and its synthetic derivatives has been documented but is rather rare. Amphetamine-related cardiac fatalities are even more rare. We present 6 cases of young persons who died unexpected after the chronic abuse of amphetamines. Death was not attributed to a lethal intoxication but to an acute myocardial necrosis, a right ventricle rupture, a cardiomyopathy, or an arrhythmia. Two of the deceased persons presented prior to their death to the emergency department, but their complaints were not considered (probably due to their young age) to be of cardiac origin. One case was a sport-related fatality where medical screening failed to identify the underlying cardiac pathology or the amphetamine abuse, and 1 case was a so-called idiopathic dilated cardiomyopathy where substance abuse was not considered by the treating physician. We think that amphetamine-associated cardiotoxicity is a rare but probably genuine entity that should be considered both in forensic and clinical/emergency medicine because of its potential medicolegal implications.

Complications during pharmacological stress echocardiography: a video-case series.

BACKGROUND: Stress echocardiography is a cost-effective tool for the modern noninvasive diagnosis of coronary artery disease. Several physical and pharmacological stresses are used in combination with echocardiographic imaging, usually exercise, dobutamine and dipyridamole. The safety of a stress is (or should be) a major determinant in the choice of testing. Although large scale single center experiences and multicenter trial information are available for both dobutamine and dipyridamole stress echo testing, complications or side effects still can occur even in the most experienced laboratories with the most skilled operators. CASE PRESENTATION: We decided to present a case collection of severe complications during pharmacological stress echo testing, including a ventricular tachycardia, cardiogenic shock, transient ischemic attack, torsade de pointe, fatal ventricular fibrillation, and free wall rupture. CONCLUSION: We believe that, in this field, every past complication described is a future complication avoided; what happens in your lab is more true of what you read in journals; and Good Clinical Practice is not "not having complications", but to describe the complications you had.

Thrombolysis increases the risk of free wall rupture in patients with acute myocardial infarction undergoing percutaneous coronary intervention.

In spite of the progress made in acute angiographic evaluation and obtaining durable reperfusion of acute myocardial infarction (AMI) in the past two decades, cardiac free wall rupture (FWR) is still one of the causes of mortality following AMI. In this study, we evaluated the role of thrombolysis in the risk of FWR in AMI patients treated with acute percutaneous coronary intervention (PCI). Among 3,786 consecutive AMI patients seen between 1985 and 2003, 3,066 patients were treated by primary PCI or rescue PCI, with or without additional thrombolysis. FWR occurred in 24 of 3,066 patients (0.8%) treated by PCI; female gender (1.4% vs 0.6%, P=0.001), age >75 years, (1.4% vs 0.6%, P=0.001) left main coronary artery (LMCA)-related infarction, (4.5% vs all other arteries, P=0.015), and thrombolytic use (3.1% vs 0.4%, P<0.001) were all associated with higher rates of FWR by univariate analysis. In patients treated with PCI and thrombolysis, FWR occurred in 2.7% with optimal PCI results but in only 4.9% if PCI was unsuccessful (P=NS). The incidence of FWR in patients with optimal PCI without thrombolysis was 0.4% (P<0.001). Multivariable analysis identified thrombolytic use (odds ratio [OR]: 8.49, 95% confidence interval [CI]: 3.66-19.7, P<0.001), LMCA-related infarction (OR: 7.06, 95% CI: 1.89-26.4, P=0.004), and female gender (OR: 3.02, 95% CI: 1.27-7.21, P=0.013) as independent predictors of FWR. Thrombolysis is one of the contributing causes of FWR in AMI patients undergoing PCI, even when PCI is successful.

Thrombospondin-2 is essential for myocardial matrix integrity: increased expression identifies failure-prone cardiac hypertrophy.

Cardiac hypertrophy can lead to heart failure (HF), but it is unpredictable which hypertrophied myocardium will progress to HF. We surmised that apart from hypertrophy-related genes, failure-related genes are expressed before the onset of failure, permitting molecular prediction of HF. Hearts from hypertensive homozygous renin-overexpressing (Ren-2) rats that had progressed to early HF were compared by microarray analysis to Ren-2 rats that had remained compensated. To identify which HF-related genes preceded failure, cardiac biopsy specimens were taken during compensated hypertrophy and we then monitored whether the rat progressed to HF or remained compensated. Among 48 genes overexpressed in failing hearts, we focused on thrombospondin-2 (TSP2). TSP2 was selectively overexpressed only in biopsy specimens from rats that later progressed to HF. Moreover, expression of TSP2 was increased in human hypertrophied hearts with decreased (0.19+/-0.01) versus normal ejection fraction (0.11+/-0.03 [arbitrary units]; P<0.05). Angiotensin II induced fatal cardiac rupture in 70% of TSP2 knockout mice, with cardiac failure in the surviving mice; this was not seen in wild-type mice. In TSP2 knockout mice, angiotensin II increased matrix metalloproteinase (MMP)-2 and MMP-9 activity by 120% and 390% compared with wild-type mice (P<0.05). In conclusion, we identify TSP2 as a crucial regulator of the integrity of the cardiac matrix that is necessary for the myocardium to cope with increased loading and that may function by its regulation of MMP activity. This suggests that expression of TSP2 marks an early-stage molecular program that is activated uniquely in hypertrophied hearts that are prone to fail.

Acute cardiac rupture during dobutamine-atropine echocardiography stress test.

We report an acute cardiac rupture during dobutamine-atropine echocardiography stress test on the sixth day after admission for an inferoposterior acute myocardial infarction complicated with mild pericardial effusion.

Fatal cardiac rupture among patients treated with thrombolytic agents and adjunctive thrombin antagonists: observations from the Thrombolysis and Thrombin Inhibition in Myocardial Infarction 9 Study.

OBJECTIVES: The purpose of this study was to determine the incidence and demographic characteristics of patients experiencing cardiac rupture after thrombolytic and adjunctive anticoagulant therapy and to identify possible associations between the mechanism of thrombin inhibition (indirect, direct) and the intensity of systemic anticoagulation with its occurrence. BACKGROUND Cardiac rupture is responsible for nearly 15% of all in-hospital deaths among patients with myocardial infarction (MI) given thrombolytic agents. Little is known about specific patient- and treatment-related risk factors. METHODS Patients (n = 3,759) with MI participating in the Thrombolysis and Thrombin Inhibition in Myocardial Infarction 9A and B trials received intravenous thrombolytic therapy, aspirin and either heparin (5,000 U bolus, 1,000 to 1,300 U/h infusion) or hirudin (0.1 to 0.6 mg/kg bolus, 0.1 to 0.2 mg/kg/h infusion) for at least 96 h. A diagnosis of cardiac rupture was made clinically in patients with sudden electromechanical dissociation in the absence of preceding congestive heart failure, slowly progressive hemodynamic compromise or malignant ventricular arrhythmias. RESULTS A total of 65 rupture events (1.7%) were reported-all were fatal, and a majority occurred within 48 h of treatment Patients with cardiac rupture were older, of lower body weight and stature and more likely to be female than those without rupture (all p < 0.001). By multivariable analysis, age >70 years (odds ratio [OR] 3.77; 95% confidence interval [CI] 2.06, 6.91), female gender (OR 2.87; 95% CI 1.44, 5.73) and prior angina (OR 1.82; 95% CI 1.05, 3.16) were independently associated with cardiac rupture. Independent predictors of nonrupture death included age >70 years (OR 3.68; 95% CI 2.53, 5.35) and prior MI (OR 2.14; 95%, CI 1.45, 3.17). There was no association between the type of thrombin inhibition, the intensity of anticoagulation and cardiac rapture. CONCLUSIONS Cardiac rupture following thrombolytic therapy tends to occur in older patients and may explain the disproportionately high mortality rate among women in prior dinical trials. Unlike major hemorrhagic complications, there is no evidence that the intensity of anticoagulation associated with heparin or hirudin administration influences the occurrence of rupture.

Late Assessment of Thrombolytic Efficacy (LATE) study with alteplase 6-24 hours after onset of acute myocardial infarction.

The effect of late thrombolysis in acute myocardial infarction (AMI)--ie, treatment beginning more than 6 h after the onset of symptoms--remains controversial. The Late Assessment of Thrombolytic Efficacy (LATE) study is a large randomised trial designed to resolve this question. 5711 patients with symptoms and electrocardiographic criteria consistent with AMI were randomised double-blind to intravenous alteplase (100 mg over 3 h) or matching placebo, between 6 and 24 h from symptom onset. Both groups received immediate oral aspirin and for later recruits intravenous heparin for 48 h was recommended. All patients were followed up for at least 6 months and 73% were followed up for 1 year. Intention-to-treat analysis of survival revealed a non-significant reduction in the alteplase group (397/2836 deaths) compared with placebo (444/2875). 35-day mortality was 8.86% and 10.31%, respectively, a relative reduction of 14.1% (95% CI 0-28.1%). Pre-specified survival analysis according to treatment within 12 h of symptom onset, however, showed a significant reduction in mortality in favour of alteplase: 35-day mortality was 8.90% versus 11.97% for placebo, a relative reduction of 25.6% (p = 0.0229, 95% CI 6.3-45.0%). Rates were 8.7% and 9.2%, respectively, for those treated at 12-24 h but subgroup analysis suggests that some patients may benefit even when treated after 12 h. Although treatment with alteplase resulted in an excess of haemorrhagic strokes, by 6 months the number of disabled survivors was the same in both treatment groups and other clinical events were observed with similar frequency in the two groups. We conclude that the time window for thrombolysis with alteplase should be extended to at least 12 h from symptom onset in patients with AMI.

Experimental pulmonary hypertension induced by constriction of the pulmonary arteries resulting in rupture or extraordinary dilatation of the right ventricle after administration of a little amount of Na2EDTA.

Our earlier studies on the hypocalcemic condition have focused on the histological distortion of the organ structure with the removal of the calcium ion from the molecular structure of acid mucopolysaccharides (AMPs); resulting in the sol-gel diversion of the matrix. Bivalent cationic materials including calcium are related not only to function but also to structural alteration of the living organism (Yamaguchi et al. 1978, 1981, 1982, 1985, 1991). The ionic shift from the structural phase to the functional phase induced a number of morphological distortions of the various organs. In the present paper, starting our research from a different experimental viewpoint, we decreased the Na2EDTA dose used to prevent the conventional typical tetanic shock which sometimes results in animal death. We expected this decreased dose to induce mild constriction of muscle cells. In our experiment, administration of a small amount of Na2EDTA intraperitoneally provoked animal death after 10 days to two weeks over a two-month period. In the initial phase of 10 days to two weeks, rupture of the right ventricular wall along the septum occurred at an anterior angle with moderate right ventricular dilatation and a remarkably thin ventricular wall. Characteristic of these cases was elastosis between the medial smooth muscle cells of the main pulmonary arteries accompanied by a severe degree of constriction. On the other hand, demonstrated in the delayed cases of between more than two weeks to two months there was severe dilatation of the right ventricular lumina with paper-like thinness of the wall. In these cases, the main pulmonary arteries showed rather slight constriction with scarce elastosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac rupture following intracoronary streptokinase.

Thrombolytic dissolution of coronary artery thrombus has added new dimensions to early myocardial infarction treatment. Reperfusion via streptokinase infusion has been shown to be beneficial; however, adverse effects are being noted. We present the case of a patient so treated who subsequently developed left ventricular free wall rupture.

[The treatment of myocardial infarct with streptokinase]. / Le traitement de l'infarctus du myocarde par la streptokinase.

The current situation concerning the use of Streptokinase in the treatment of recent myocardial infarction does not make it possible to draw any definite conclusions with regard to its therapeutic value:--mortality would not appear to be significantly modified in the majority of series;--the occurrence rate of major complications during the acute phase is not notably altered but it seems possible that the electrocardiographic course of the necrosis is more favourable under the influence of Streptokinase when treatment is begun early. The long term course cannot be assessed. Finally, it is certain that the tolerance of Streptokinase therapy has been good in all the published series. In particular, Streptokinase does not appear to have been associated with severe haemorrhagic complications nor a higher prevalence of cardiac rupture.