SUMMARYForty years ago, after the establishment of coronary care units, a significant decrease in mortality of acute myocardial infarction was noted. Twenty years ago, the breakthrough of thrombolysis realized once again a significant decrease in mortality. In this study we compare, in a rather small community hospital, the mortality and safety of thrombolytic therapy in acute myocardial infarction with a more conventional, conservative medical therapy.We examined all cases of acute myocardial infarction between 1978 up to 1998 inclusive, concerning treatment and mortality rate after a six month period. To be included in the study, acute myocardial infarction had to fulfill particular inclusion criteria. A total of 1863 cases of acute myocardial infarction were included.The mortality rate of patients with acute myocardial infarction treated with thrombolytic agents was strikingly lower and statistically very significantly different (p < 0.001) in comparison with the mortality rate of patients treated with heparin or coumarine derivatives.The mortality rate dropped from 10.57% in the coumarine group and from 14.95% in the heparin group to 5.41% in the alteplase group, to 4.95% in the anistreplase group and 4.00% in the streptokinase subgroup.The complications directly connected to the treatment did not seem to be different between the five groups, and they were also not more frequent by using thrombolytic agents.In the last 20 years, better preventive measures (life habits, diet, medication) and trials to better control the risk factors have not influenced greatly the average amount of cholesterol in patients with an acute myocardial infarction. Also the percentage of patients with high blood pressure has hardly decreased over the last 20 years.The mortality associated with acute myocardial infarction has decreased significantly with the use of thrombolytics. In most cases, thrombolytics are administered routinely and safely. In this way, they are the first choice therapy for myocardial infarction in smaller hospitals.
The use of yew leaves (Taxus Baccata) as a means of deliberate self-harm is infrequent. The potent effect of the toxin is primarily cardiac and results in rhythm alterations and ultimately ventricular fibrillation. As there is no known antidote, and classic antiarrhythmic therapy proves to be ineffective, a prompt diagnosis is of great importance as immediate supportive action is the only valuable alternative. This case describes a 43-year-old women who attempted suicide by ingesting the leaves of Taxus Baccata. We discuss the effects and the difficulty of treatment associated with yew leaf poisoning.
Transcatheter closure of a patent foramen ovale (PFO) offers a valuable alternative to surgery in selected patients with presumed paradoxical embolism. Like for all other devices, several complications have been described. Although the majority of these complications are caused by technical problems of the device itself, thrombosis is a relatively infrequent but feared finding, as it may result in recurrent embolic events and persistent neurological deficits. The majority of the complications after implantation are dealt with by surgical removal of the device and subsequent surgical closure of the PFO. The present case report describes biatrial thrombosis of a PFO device that was successfully treated with thrombolytics and GP IIb/IIIa receptor blockers. In stable patients, this pharmaco-therapeutic approach should be attempted to save the thrombosed PFO device and could therefore offer a valuable alternative to surgical removal of the device.
Sudden death is a tragic fact, unexpectedly arising in all age groups. Ventricular arrhythmias are the main cause. At the end of a maximal exercise test more ventricular premature beats were noted in a group of well trained triathletes compared with a similar control group. The etiology is multifactorial. When these ventricular premature beats are associated with specific structural and functional heart adaptations, echocardiographically and electrocardiographically well-documented, then those ‘banal’ ventricular premature beats cannot longer be considered as a physiological phenomenon. In these circumstances the involved subject is a candidate for dangerous arrhythmias and ‘sudden cardiac death’. Purpose: The principal cause of ‘Sudden cardiac death’ is ventricular arrhythmias. We explore the incidence of ventricular premature beats (VPB) in triathletes, who engage in enforced endurance sports. Methods: Fifty-two triathletes were compared with twenty-two control subjects with comparable anthropometric parameters in function of structural and functional cardiac adaptations. Maximal exercise tests were conducted on a stationary bicycle and a treadmill. During the last two minutes of each test, the VPB were registered. Results: Statistically significant differences emerged in the cardiac structure and function between the triathletes and the controls. There were signs of cardiac hypertrophy and arguments for a supernormally diastolic left ventricular function in the triathletes. The performance capacity was also significantly higher in the triathletes. The maximal heart rate was significantly higher in the control group. The number of VPB was significantly higher in the triathletes. The increased risk of VPB in the triathlon group is caused by several factors: the degree of cardiac hypertrophy, the increased diastolic reserve, the duration of the exercise, the existence of an aortic insufficiency jet and some specific electrocardiographic findings. Conclusions: The triathlete has an increased risk of VPB during maximal efforts. We doubt the traditionally accepted view of the physiological nature of those VPB and suspect that the limit of physiological cardiac adaptations to sport efforts is exceeded with the appearance of VPB. The triathlete with VPB and with specific electrocardiographic and echocardiographic findings is a candidate for ‘sudden cardiac death’.
"Sudden cardiac death" in seemingly healthy, active, and asymptomatic people has always been a tragic fact and is now occurring more frequently. Thus, the preventive detection of "subjects at risk" becomes a priority. A traditional resting electrocardiogram can sometimes give useful indications. Fifty-two competitive triathletes were compared with 22 control persons with similar anthropometric parameters. All subjects underwent the same noninvasive cardiac exploration with electrocardiography, bidimensional echo-Doppler examination, and maximal spiroergometric exercise tests, on a stationary bicycle as well as on a treadmill. In the triathletes we noted manifest signs of eccentric as well as concentric left ventricular hypertrophy with arguments for a supernormal diastolic left ventricular function, with important hemodynamic adjustments and with consequences on the resting electrocardiogram. We described "ten commandments" in evaluating the resting electrocardiogram of healthy competitive athletes. We suspect that the occurrence of ventricular premature beats at peak load of a maximal exercise could be the first expression of a pathological cardiac adaptation to sports activities. The resting electrocardiogram can show interesting details in detecting the "subjects at risk" for problems such as possible lethal arrhythmias and "sudden cardiac death." The analysis of the four subgroups of triathletes compels us to feel dubious about the "athletic heart syndrome" as a physiological entity. In several cases the "athletic heart" is possibly a transitional situation to a pathological hypertrophic and dilated cardiomyopathy.
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