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Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined the effects of ventricular dilatation on epicardial refractoriness and ventricular fibrillation threshold (VFT) in the isolated, retrograde-perfused rabbit heart. Ventricular size was modified by acutely changing the volume of a fluid-filled balloon secured within either the left or right ventricle. Left ventricular dilatation (to an end-diastolic pressure of 30-38 mmHg) significantly decreased left ventricular effective refractory period (ERP) and myocardial wavelength (calculated as ERP x conduction velocity). Left VFT (determined by scanning the vulnerable period with a train of pulses) decreased from 6.4 +/- 0.9 to 4.4 +/- 0.5 mA; P < 0.01) with left but not right ventricular dilatation. Right ventricular dilatation was associated with a decrease in the right ventricular ERP and myocardial wavelength, and right VFT decreased from 13.6 +/- 1.8 to 4.1 +/- 0.3 mA (P < 0.01). Changes in VFT correlated with the decrease in local refractoriness and shortening of local excitation wavelength.
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PMID:Effect of acute ventricular dilatation on fibrillation thresholds in the isolated rabbit heart. 141 78

In the first few hours after the onset of coronary occlusion the infarct zone stretches due to myocyte slippage. Subsequently the noninfarct zone develops volume overload hypertrophy with series addition of new sarcomeres and fibre elongation. Dilatation is detrimental as it increases ventricular wall stress and oxygen demand, and re-entry of electrical impulses may be influenced by stretching of the ischaemic scar resulting in ventricular fibrillation. Left ventricular remodelling and dilatation is a progressive process which begins early and continues in the months after infarction. The major determinants of the extent of remodelling are infarct size and patency of the infarct-related artery. Late reperfusion may reverse initial infarct dilatation and decrease left ventricular volumes by inducing calcium-activated contracture of the actomyosin complex. Expansion may also be inhibited by acceleration of healing, splinting of the infarct zone by salvage of subepicardial cells, and blood in the coronary arteries and veins supporting the infarct zone. End-systolic volume is the strongest predictor of long-term prognosis after infarction. A number of therapies including thrombolysis, angiotensin-converting enzyme (ACE) inhibition and nitrates have been shown to decrease left ventricular dilatation. The optimal time for commencement, dose, duration and the effects of combinations of therapy are yet to be determined.
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PMID:Remodelling of the heart after myocardial infarction. 144 47

Ventricular fibrillation and sudden death are rare phenomena in nonischemic ventricular arrhythmia, particularly in arrhythmogenic right ventricular cardiomyopathy. In most instances electrophysiologic studies help to assess the risk of sudden death, but sometimes programmed ventricular stimulation is unsuccessful. Among 48 patients with ventricular fibrillation (n = 9) and sustained (n = 25) and nonsustained (n = 19) ventricular tachycardia, invasive and noninvasive diagnostic tests (coronary angiography, biventricular angiography, programmed ventricular stimulation, and echocardiography) were performed to obtain more information about the underlying heart disease. In 43 patients (90%) arrhythmogenic right ventricular cardiomyopathy was diagnosed with segmental hypokinesia (n = 31) and diffuse hypokinesia (n = 12) of the right ventricle. In patients with documented ventricular fibrillation, the right ventricular ejection fraction was lower (30.8% vs 47.8% and 45.9%, respectively) and multisegmental contraction impairment of the right ventricle was significantly more frequent (p less than 0.001). Additional left ventricular abnormalities and right ventricular dilatation were not significant parameters for identifying high-risk patients. In addition to programmed ventricular stimulation, quantitative analysis of the results of right and left ventricular angiography contributes to risk assessment in patients with nonischemic ventricular arrhythmia.
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PMID:Risk assessment in nonischemic ventricular arrhythmia by left and right ventriculography. 161 93

1. The circulating and tissue renin-angiotensin systems (RAS) contribute importantly to cardiovascular homeostasis. Systemic and/or local activation of the RAS is seen in many pathological conditions of the cardiovascular system (e.g. hypertension and congestive heart failure). Increased angiotensin production participates in the pathophysiology of these and other disease states. Accordingly, inhibitors of the renin angiotensin system have a broad spectrum of therapeutic efficacy. 2. Angiotensin-converting enzyme (ACE) inhibitors are effective antihypertensive agents that do not adversely affect serum lipid levels. In addition, they reduce left ventricular hypertrophy. 3. ACE inhibitors cause coronary vasodilation and reduce ventricular work and wall stress. They have been shown to reduce experimental infarct size and to increase anginal threshold in humans. 4. After experimental or human myocardial infarction that results in significant left ventricular dysfunction, ACE inhibitors prevent ventricular dilatation and development of congestive heart failure, and may improve survival. 5. ACE inhibitors can prevent ventricular fibrillation and contractile impairment (stunned myocardium) associated with reperfusion injury after experimental myocardial ischaemia. 6. ACE inhibitors reduce preload and afterload, improve exercise capacity, reduce ventricular arrhythmias, and improve patient survival in clinical cardiac failure. 7. Taken together, inhibition of the RAS may potentially result in primary as well as secondary protective effects on the cardiovascular system.
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PMID:Clinical implications for therapy: possible cardioprotective effects of ACE inhibition. 269 Sep 9

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

This study examined inducibility of ventricular tachyarrhythmias in turkeys with and without naturally occurring dilated cardiomyopathy. Using a transvenously positioned electrode catheter, 32 cardiomyopathy and 12 control unsedated turkeys aged 2 to 4 months were studied by right ventricular endocardial extrastimulus testing at basic pacing cycle lengths of 200 and 170 ms with both 1 and 2 extrastimuli and burst pacing at progressively shorter cycle lengths (200 to 100 ms). Following study, a dilatation index (determined as the ratio of left ventricular endocardial and epicardial diameter at level of the apex-base midpoint) was utilized to assess the functional severity of cardiomyopathy. All control turkeys had a dilatation index less than 0.3. In cardiomyopathic turkeys, dilatation index was normal (less than 0.3) in 3/32, showed mild to moderate dilatation in 25/32 (0.3 to 0.6), and severe dilatation in 4/32 (greater than 0.6). Results showed no difference in right ventricular effective or functional refractory periods between control and cardiomyopathic turkeys. Control turkeys had no inducible ventricular tachyarrhythmias, but 16/32 cardiomyopathic turkeys (p less than 0.005) had inducible ventricular tachyarrhythmias, consisting most frequently of two beats of rapid ventricular tachycardia supervened by ventricular fibrillation. In the cardiomyopathic turkeys, inducible tachyarrhythmias occurred in 1/3 with normal dilatation index, in 11/25 with mild to moderate dilatation, and in 4/4 with severe dilatation. Thus, inducibility of ventricular tachyarrhythmias in cardiomyopathic turkeys is closely associated with increasing ventricular dilatation, but does not correlate with altered right ventricular refractoriness. This model may be suitable for studying the relationship between ventricular tachyarrhythmias and cardiomyopathy.
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PMID:Inducible ventricular arrhythmias in a naturally occurring model of cardiomyopathy. 648 34

Electrophysiological studies showed ventricular tachycardia in five patients (four male, one female) with isolated right ventricular dilatation. All had been asymptomatic before the onset of palpitation which had developed in adolescence or early adult life. Tachycardia had been associated with syncope in four patients, and three had been resuscitated from ventricular fibrillation before investigation. The electrocardiogram during ventricular tachycardia showed a left bundle branch block pattern, and endocardial mapping at electrophysiological study confirmed the right ventricular origin. The presenting tachycardia could be induced in all patients by programmed stimulation, and in three patients ventricular tachycardia of differing configuration could be induced, but the right ventricular origin and left bundle branch block pattern were maintained. In two patients ventricular tachycardia degenerated into ventricular fibrillation. Cineangiography, cross sectional echocardiography, and multigated radionuclide angiography confirmed the dilated abnormal right ventricle while indicating that left ventricular function was normal. On resting electrocardiograms T wave inversion over the right precordial leads was the sole abnormality. There were no signs of right heart failure and exercise tolerance was normal. Four patients have received maintenance treatment with antiarrhythmic drugs, and one had undergone operative mapping and ablative surgery. Thus ventricular tachycardia complicating right ventricular dilatation may be associated with serious symptoms and ventricular electrical instability; and in adults it may be suspected on clinical grounds by inverted T waves in the right precordial leads.
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PMID:Ventricular tachycardia of left bundle branch block configuration in patients with isolated right ventricular dilatation. Clinical and electrophysiological features. 668 16

A 27-year-old man with typical mitral leaflet prolapse syndrome was under medical care for eight years with ventricular arrhythmias resistant to various antiarrhythmic drugs. He was started on digoxin, 0.25 mg daily, because of echocardiographically demonstrated left ventricular dilatation and functional impairment; he died of ventricular fibrillation 15 days later.
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PMID:Fatal ventricular fibrillation after treatment with digoxin in a 27-year-old man with mitral leaflet prolapse syndrome. 729 27

The history of an 18-year-old male with hypertrophic cardiomyopathy (HCM) and ventricular dilatation is presented and the literature on systolic dysfunction and ventricular dilatation in patients with HCM is statistically analyzed in search of risk factors. The patient was followed for 7 years when he developed recurrent ventricular fibrillation, left ventricular dilatation and low cardiac output. An automatic cardioverter-defibrillator was implanted but the patient died of electro-mechanical dissociation. In order to define risk factors for systolic dysfunction and ventricular dilatation in HCM, the literature data of 17 patients with this complication were compared to a group of 139 consecutive patients with HCM from our hospital. The risk factors identified were a more markedly increased septal (20.1 vs. 18.0 mm, P < 0.05) and posterior wall thickness (13.6 vs. 11.0 mm, P < 0.001) in the patients subsequently developing systolic dysfunction and ventricular dilatation, whereas age, sex and the ratio between septal and posterior wall thickness were not significantly different between the two groups. A severely increased ventricular mass appears to be a risk factor for the development of systolic dysfunction with ventricular dilatation in HCM. Prognosis is usually poor and the reported case showed fatal ventricular arrhythmia despite the implantation of an automatic cardioverter-defibrillator.
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PMID:Risk factors for systolic dysfunction and ventricular dilatation in hypertrophic cardiomyopathy. 807 68

Potassium depletion has been implicated in the genesis of ventricular arrhythmias, especially in patients with congestive heart failure, but the nature of this interaction is unknown. We studied the electrophysiological effects of varying concentrations of extracellular K+ in 24 isolated, retrogradely perfused rabbit hearts. The left ventricular cavity was dilated with a fluid-filled balloon. Left ventricular effective refractory period decreased significantly (from 119 +/- 3 to 105 +/- 3 ms) with ventricular dilatation but was not influenced by K+ concentration. Conduction velocity was not changed by dilatation but was decreased by hypokalemia (81 +/- 2 cm/s, K+ = 4.9 mM; 75 +/- 2 cm/s, K+ = 3.5 mM; 70 +/- 2 cm/s, K+ = 2.5 mM; P < 0.05). No ventricular arrhythmias were induced in undilated hearts at a K+ concentration of 4.9 mM. Induced ventricular fibrillation was more frequent (38%; P < 0.01) in the dilated heart and increased markedly (92%; P < 0.01) with coexisting hypokalemia. The incidence of induced fibrillation was highly correlated with the wavelength of the ventricular impulse (wavelength = refractory period x conduction velocity). Thus dilatation and hypokalemia have very different electrophysiological effects that can interact synergistically to predispose the heart to reentrant arrhythmias in this model.
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PMID:Interaction of hypokalemia and ventricular dilatation in isolated rabbit hearts. 823 65


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