[The electrocardiographic diagnosis of ventricular hypertrophy in the presence of a bundle branch block or a fascicular block].
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Biomedical subjects
Publications and source records attributed to M Gertsch.
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Intravenous amiodarone has a clear anti-arrhythmic effect on induced sustained ventricular tachycardia (VT) in pigs with subacute myocardial infarction. Degeneration of the VT into ventricular fibrillation is almost abolished, and conversion of VT into sinus rhythm by programmed stimulation is enhanced.
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Sudden death and its consequences in patients with coronary artery disease have stimulated research in this field. In the light of the literature an attempt is made to outline the present state of diagnosis and especially longterm medical treatment in ventricular arrhythmias. New morphological electrocardiographic criteria for differentiation between supraventricular and ventricular tachycardias are mentioned. It seems to be the general opinion that ventricular arrhythmias in persons with otherwise normal cardiac findings have a good prognosis and do not need drug therapy. Drug therapy of ventricular arrhythmias in patients with cardiac disease sets out to lower the incidence of sudden death and should be used only for dangerous arrhythmias (ventricular premature beats of Lown classes 3 to 5) and in patients with significant heart disease. Toxic factors and arrhythmogenic properties and other side effects of the antiarrhythmic drugs should be considered. The subdivision of these drugs into classes I to IV according to their effect on the action potential fo the isolated muscle fiber of the heart is briefly reviewed. Standard doses and important side effects of drugs generally used in the treatment of ventricular arrhythmias are given. Drug testing with invasive cardiac stimulation is complicated and expensive and is performed in a few specialized centers only. Oral drug testing with monitoring of the drug effect by ambulatory electrocardiography and measurement of blood levels usually permits the correct choice of an antiarrhythmic drug. For practical use a somewhat simplified method of oral drug testing is proposed in which rhythm strips replace the ambulatory ECG. This modification does not sufficiently allow for the spontaneous variability of ventricular ectopy, but will probably permit some guidance of the antiarrhythmic therapy. It is obvious that the practical application of the new concepts in the management of ventricular arrhythmias is difficult. Finally, the therapy of supraventricular tachyarrhythmias is briefly summarized.
We examined a 29-year-old woman with nemaline myopathy that appeared as cardiomyopathy. Clinical examination showed dilated cardiomyopathy, but no neuromuscular abnormalities of the skeletal muscles. Electromyography showed neither neurogenic nor myopathic abnormalities. A biopsy specimen from the quadripecs muscle showed typical nemaline bodies in about 50% of the muscle fibers. The patient died six months later of biventricular heart insufficiency. Autopsy revealed nemaline bodies in the working and conducting tissues of the myocardium. Earlier, the patient's mother and one of her sisters died unexplained, sudden deaths at the ages of 47 and 37 years, respectively. Sections of the myocardium taken from the sister at autopsy were available, and also disclosed nemaline bodies after restaining with trichrome.
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A study was designed to examine ventricular arrhythmias in the acute phase of experimental myocardial infarction in the pig and to evaluate possible antiarrhythmogenic influence of the beta-adrenergic blocking drug pindolol (Visken) and the calcium antagonist Ro 11-1781. Ventricular fibrillation (VF) occurred in 17 of 18 animals, in 4 almost immediately after coronary occlusion and in 12 with a delay of about 17 min. VF was almost always induced by episodes of ventricular tachycardia (VT) which were started by single ventricular premature beats (VPBs). VPBs occurred in 3 phases, whereas VT and VF coincided only with phase 1 and phase 3. The prematurity index QR/QT of single VPBs decreased significantly with time after coronary occlusion. The beta-adrenergic blocking drug pindolol and the calcium antagonist Ro 11-1781 did not prevent VT or VF.
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A short period of myocardial ischemia induced by temporary ligation of 2 min duration prior to occlusion of the left anterior descending branch of the left coronary artery (LAD) in the pig does not have a beneficial effect on epicardial ST-segment alterations or on the incidence of ventricular fibrillation. One-stage ligation therefore seems to be the procedure of choice in occluding the porcine LAD. In 14 of 24 animals an isolated alternans of the ST-T segment was observed during the first few minutes of occlusion. Reperfusion after 60 min caused temporary increase of the ST-segment alterations, in contrast to the findings in the dog, where revascularization causes prompt return of the ST-segment to the pre-occlusion level. In addition, ectopic rhythms were frequently observed after removal of ligation.
The initiation and termination of ventricular tachycardia by means of programmed orthorhythmic endocardial stimulation has been studied in pigs with subacute experimental myocardial infarction. Successful stimulation implied limited variation of the number, interval, prematurity and intensity of electrical impulses.
100 ECGs with left axis deviation have been analyzed with respect to left anterior fascicular block (LAFB). On the basis of conventional criteria LAFB was diagnosed in 59 cases, but could be rules out in 26. Of the remaining 15 ECGs which at first seemed doubtful, 4 were identified as LAFB on the basis of a new criterion: duration of qR in a VL at least 40 msec longer than in V6.
The sick sinus syndrome is caused by dysfunction of the sinus node and includes various forms of arrhythmia. In its chronic form the underlying disease may affect not only the sinus node but also the atrial, junctional and intraventricular conduction tissue. The most important clinical symptoms are, in decreasing order, dizziness, syncope, palpitations, cardiac failure, systemic embolism, and cerebrovascular insult. The main diseases causing dysfunction of the sinus node are coronary heart disease, myocarditis, and rheumatic fever. The diagnosis is based on history, clinical findings, ECG, specific provocative tests and, if necessary, long-term ECG monitoring. The sick sinus syndrome is most frequently seen in patients aged over 50 years. Treatment with drugs alone, such as atropin, catecholamines, digitalis or antiarrhythmic drugs is often difficult becuase of the frequent changes between bradycardic and tachycardic arrhythmia. In chronic and progressive cases, the best treatment is implantation of a cardiac pacemaker.
A case of myocardial infarction in a newborn, most probably consecutive to air embolism, is described. The acute episode occurred immediately after the removal of a venous umbilical catheter. The infant survived, without clinical evidence of cardiac impairment 14 months later. However, he developed signs of a spastic cerebral palsy.
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