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Query: UMLS:C0042510 (ventricular fibrillation)
 10,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The success of aneurysmectomy in abolishing recurrent ventricular tachycardia or ventricular fibrillation has not been clearly defined. Ten patients who underwent aneurysm resection to control ventricular arrhythmias were studied before and an average of 19 (4 to 42) months following operation. All patients had moderate to large aneurysms and four had asynergy in adjacent segments. Of four patients with significant stenosis in vessels not supplying the aneurysm, three had aortocoronary bypass grafts in addition to their resection. Ambulatory Holter monitoring and a graded exercise test were performed in all patients postoperatively. There was no operative mortality. Two patients who did not have associated revascularization procedures died suddenly 1.5 and 7 months postoperatively. Of the eight survivors, despite clinical improvement, the Holter ECG revealed runs of ventricular tachycardia in three patients and frequent multifocal ventricular extrasystoles in the other five patients. No correlation was found between recurrence of the ventricular arrhythmias and aneurysm size, contraction pattern of other myocardial segments, extent of coronary disease, or the presence of congestive heart failure. In conclusion, aneurysmectomy does not abolish ventricular tachyarrhythmias and probably should be reserved for patients who remain symptomatic despite an adequate medical trial. The persistence of complex arrhythmias following operation warrants a close follow-up in these patients.
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PMID:Long term follow-up of aneurysmectomy for recurrent ventricular tachycardia or fibrillation. 30 2

The presented analysis deals with the physiopathological mechanisms of the debelopment of postinfarction cardiac insufficiency and the clinical peculiarities of its manifestations. It is emphasized that the leading cause of cardiac insufficiency consists in a reduction of the contractile function of the left ventricular myocardium due to the development of asynergy in the cicatrical zone. The addition of several accompanying factors, such as heart mitralization, tachysystolic form of ventricular fibrillation, repeated infarction with a growing asynergic zone, aggravate the course of cardiac insufficiency providing for the development of hypertension in the general circulation system.
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PMID:[Cardiac insufficiency in ischemic heart disease]. 78 66

To evaluate the association between left ventricular false tendon (LVFT) and ventricular arrhythmias in acute myocardial infarction (MI) on the 1-st day of acute MI 71 patients were examined by 24-hour ECG-monitoring and M-mode, two-dimensional, Doppler echocardiography. LVFT was detected in 30 patients (42.3%). The frequency of left ventricular fibrillation, the number of patients with multiform ectopic ventricular beats (EVB), the number of single and pair EVB and runs of ventricular tachycardia were greater in group of patients with LVFT. 37 patients had Lown grades 1-2 (A) of arrhythmias, 34 patients had grades 3-5 (B). LVFT was revealed in four patients in group A (10.8%) and in 27 patients in group B (76.5%, p < 0.001). There were no significant differences between groups in left ventricular asynergy area and wall motion score, left and right ventricular, left atrium dimensions, left ventricular contractility indices, left ventricular walls thickness, frequency of mitral regurgitation. Multifactor analysis has shown significant relationship between Lown's class value and LVFT (p < 0.0001), Lown's class and arterial hypertension (p = 0.0376). Other 17 clinical factors were not connected with Lown's class value. Thus, LVFT was associated with severe ventricular arrhythmias in patients with AMI. This fact can be used as a predictor of these disturbances.
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PMID:Relationship between ventricular arrhythmias and left ventricular false tendons in acute myocardial infarction. 129 Jun 56

Out of 178 consecutive patients with acute inferior wall myocardial infarction submitted to technetium-99 m pyrophosphate scintigraphy, 49 (27.5%) were found to have concomitant right ventricular infarction. Gated blood pool scans showed right ventricular abnormalities in 21 out of 26 patients who were submitted to this investigation (right ventricular asynergy: 16 cases; right ventricular dilatation: eight cases; decreased right ventricular ejection fraction: 16 cases). Complications were common in the acute stage. Shock was noted in 19 cases (eight related to bradycardia, three related to relative hypovolaemia and eight instances of true cardiogenic shock). Atrial fibrillation (seven patients), ventricular fibrillation (eight patients) and severe atrioventricular conduction disorders (13 patients) were also frequent. In spite of this, the in-hospital mortality was low: three deaths occurred (6.1%), one from heart failure, two others from posterior septal rupture. All patients were followed up for one year or more. Six additional deaths were noted (three from left cardiac failure, two from recurrent anterior wall infarction and one from massive pulmonary embolism). Clinical assessment, haemodynamic measurements and gated blood pool scans showed significant improvement of right ventricular function with return to normal in those cases with small right ventricular infarcts as judged from technetium-99 m pyrophosphate scintigraphy. In spite of the complications seen in the initial period, patients with a right ventricular infarction have a good overall prognosis and the long-term outcome, primarily determined by the left-sided lesions, is often favourable.
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PMID:Right ventricular myocardial infarction diagnosed by 99 m technetium pyrophosphate scintigraphy: clinical course and follow-up. 629 41

Electrocardiographic abnormalities had been reported, in patients with subarachnoid hemorrhage, with variable percentage from 2% to 91%, according to several studies. The most common changes are T wave inversion, ST segment elevation or depression, QT prolongation, U waves, atrial flutter and fibrillation, ventricular fibrillation, supraventricular tachycardia, premature atrial and ventricular contractions. These findings occur within the first forty-eight hours after the onset of the symptoms; they usually are benign and transient. In a small percentage of cases generally in severe ESA, the ECG changes are associated with ventricular asynergy, coronary vasospasm or subendocardic necrosis. The arrhythmias could be produced either by autonomic discharges to the heart, during increased sympathetic activity due to ESA, or by a damage of cerebral areas with arrhythmogenic capacity. The importance of ECG abnormalities towards mortality and morbidity in patients with ESA has not yet been cleared; however, a careful monitoring is recommended to prevent severe cardiac complications and to obtain an indirect, further evaluation of the neurologic pathology.
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PMID:[Subarachnoid hemorrhage and the heart]. 977 66

Subarachnoid hemorrhage (SAH) due to aneurysmal rupture is frequently complicated by cardiopulmonary episodes, including sudden death. We investigated the pathogenesis of cardiopulmonary complications from clinical observation of 715 cases with SAH. There was transient left ventricular asynergy in 9.4% (67/715) of the cases, which consisted of mechanical heart failure and myocardial necrosis. Plasma catecholamine concentration was higher in these patients compared with those without left ventricular asynergy. Transient left ventricular asynergy was considered to result from myocardial derangement: "a panic myocardium," due to a sudden burst of catecholamine. Concerning arrhythmia in SAH, cases with life-threatening arrhythmia, such as ventricular tachycardia or ventricular fibrillation, had higher concentrations not only of plasma catecholamine but also of serum CK-MB, myosin light chain and troponin T, compared with patients who had no ventricular arrhythmia. This implies that life-threatening arrhythmia in SAH would result from myocardial damage due to catecholamine. We devised a novel animal model of SAH in order to clarify the relation between sympathetic nervous activity and myocardial damage immediately after the onset of SAH. The animal experiments showed that sympathetic nervous activity as well as cardiac contractility were transiently elevated, but cardiac function subsequently declined. Serum CK-MB was increased from the onset of SAH and a high value was maintained throughout the entire experimental period. In conclusion, extraordinary transient enhancement of sympathetic nervous activity induces myocardial damage resulting from what is characterized by "a panic myocardium."
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PMID:Subarachnoid hemorrhage and myocardial damage clinical and experimental studies. 1073 53

An 81-year-old woman was admitted with chest pain. An electrocardiogram demonstrated ST segment elevation in leads II, III and aVF, and echocardiography revealed left ventricular apical asynergy with a left-to-right ventricular shunt. Meanwhile, emergent coronary angiography showed no significant coronary artery stenosis, whereas left ventriculography indicated apical ballooning and a left-to-right ventricular shunt. We therefore diagnosed the patient with Takotsubo cardiomyopathy complicated by ventricular septal perforation and cardiogenic shock. An electrocardiogram disclosed a prolonged QT interval over time, and the patient became hemodynamically stable under treatment with inotropes; however, she suddenly developed fatal ventricular fibrillation three days after hospitalization. Takotsubo cardiomyopathy complicated by ventricular septal perforation is a critical condition that requires careful monitoring.
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PMID:Critical takotsubo cardiomyopathy complicated by ventricular septal perforation. 2574 91