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Biomedical subjects

M Zehender

Publications and source records attributed to M Zehender.

94 records · Page 6Linked to original sources

Clinical, angiographic, and electrophysiologic findings in patients with aborted sudden death as compared with patients with sustained ventricular tachycardia after myocardial infarction.

After the acute phase of myocardial infarction, patients who develop sustained ventricular arrhythmias present with either sudden death or ventricular tachycardia (VT). Although current evidence suggests that VT frequently precedes ventricular fibrillation (VF) in patients presenting with sudden death, the factors resulting in rapid deterioration of VT to VF have not been delineated in humans. To determine whether left ventricular function, coronary anatomy, or electrophysiologic characteristics could differentiate patients with sudden death from those with VT without sudden death, we compared results of cardiac angiography and programmed electrical stimulation in 42 patients referred for evaluation of sustained VT or surviving "aborted" sudden death for more than 9 days after myocardial infarction. By univariate analysis there were no differences between patients with sudden death and those with VT in age, time from myocardial infarction to VT or sudden death, ejection fraction (0.31 +/- 0.12 vs 0.29 +/- 0.09), or the number of patients with a major area of contracting myocardium supplied by an artery with a 50% or greater or a 70% or greater stenosis (84% vs 64% and 68% vs 41%). Thirty-six percent of patients with sudden death but no patient with VT had two separate areas of infarction. During programmed electrical stimulation, a sustained ventricular arrhythmia was initiated in 100% of patients with VT and 73% of patients with sudden death and rapidly produced syncope in 67% of patients with sudden death but in only 5% of those with VT. This difference was due to the more frequent initiation of rapid polymorphic VT or VF (27% of patients) and to the shorter VT cycle length (242 +/- 31 vs 319 +/- 69 msec) when monomorphic VT was induced in the group with sudden death. No difference was found in the number of extrastimuli required for initiation of a sustained ventricular arrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

[Arrhythmias in subjects with a healthy heart].

Of 350 patients who had extensive non-invasive and invasive cardiological diagnostic tests, 56 had completely normal results. 24-hour ECG monitoring of the latter revealed the following ventricular arrhythmias-ventricular extrasystoles (VES): 36% without, 23% with rare ones (less than 30/h), 5.4% with more than 30/h, 25% with polytopic VES, 7.1% with paired VES and 3.6% with ventricular tachycardia. There was no preferential VES pattern. Mean duration of VES was 0.15 s. There were no VES with a prematurity index of less than 1. Extending ECG monitoring to 96 hours (10 persons without heart disease) did not reveal any more significant VES, but registering for less than 24 hours definitely underestimated the frequency of VES in persons without heart disease. In those without angiographic evidence of heart disease 36% had complex and 5.4% frequent VES. Complex arrhythmias, however, are rare in the individual subject and generally not accompanied by frequent VES. Frequent complex arrhythmias or both frequent and complex arrhythmias, as well as VES with a prematurity index less than 1, are suggestive of organic heart disease.

Adult↗

Effect of tetrodotoxin, lidocaine, and quinidine on the transient inward current of sheep Purkinje fibres.

The effect of tetrodotoxin (TTX), lidocaine, and quinidine on the transient inward current (TI) was studied in voltage-clamped sheep cardiac Purkinje fibres. The TI was induced by elevation of extracellular Ca or addition of strophanthidin. Reduction of external Na had a biphasic effect on the steady state TI magnitude; a moderate (less than 50%) reduction of external Na had an enhancing effect on the TI; a further decrease of extracellular Na was accompanied by a decline of TI amplitude. The TI could not be induced in Na-free medium (external Ca less than or equal to 9.0 mM). TTX, lidocaine, and quinidine reduced the magnitude of the TI in a dose-dependent way. The blocking effect of these agents could be compensated for by a moderate (less than 50%) reduction of external Na or an elevation of extracellular Ca. It is suggested that the blocking effect of TTX, lidocaine, and quinidine on the TI is due to a reduction of intracellular Na, which causes a decay of intracellular Ca via the Na-Ca exchange mechanism.

Animals↗