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 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The paper proposes new criteria for differential diagnosis of myocardial "focal scarring" and "++pseudo-scarring" changes in various cardiac abnormalities and homogeneous morphological alterations in the ventricular complex on ECG (the QS, Qr-type abnormalities of the R line) by using the findings of 35 lead ECG mapping (PM-35). ECG-12 and PM-35 were analysed in 427 patients, including those with coronary heart disease (n-122), arterial hypertension and aortic malformations (n-130), dilated cardiomyopathy, congenital cardiac disease (n-175). Electrocardiographic signs of focal scarring lesions were revealed in all the cases with coronary heart disease and 66 with myocardial hypertrophy. The total value of ST segment depression and the sum of Q wave squares in three to five vertical mapping columns were found to be the most significant differential and diagnostic criterion. When scars and ++pseudo-scars were differentiated, a sensitivity of 75% was obtained at a specificity of 87%.
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PMID:[Use of integral indicators of precordial mapping in differential diagnosis of focal-cicatricial lesions of the myocardium]. 223 65

Elevated systemic vascular resistance in heart failure causes further depression of cardiac function. Decreased systemic vascular resistance, on the other hand, is associated with an improvement in cardiac performance. Thus, peripheral vasodilators, irrespective of their mechanism of action, have the potential to improve cardiac function in heart failure. Increased peripheral vascular tone appears to result from a number of interrelated neuroendocrine dysfunctions--an activated renin-angiotensin-aldosterone system, inappropriate release of arginine vasopressin, and enhanced systemic and cardiac sympathetic activity (indicated by increased levels of circulating norepinephrine and markedly increased cardiac norepinephrine release). Augmented sympathetic activity may not only increase systemic vascular resistance but can also induce myocardial cellular dysfunction. Furthermore, downregulation of cardiac beta-adrenoceptors may contribute to inadequate cardiac performance. Reduction of sympathetic tone and upregulation of the beta-adrenoceptors is the rationale for beta-blocker therapy in heart failure and, indeed, cardioselective beta-blockers improve cardiac function in some patients with dilated cardiomyopathy. Third-generation beta-blockers, such as celiprolol, possess both cardioselective and peripheral vasodilatory properties and are therefore potentially beneficial in heart failure.
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PMID:Potential use of third-generation beta-blockers in heart failure. 248 86

The long-term prognosis for 314 patients with hypertrophic cardiomyopathy (HCM) and 82 with dilated cardiomyopathy (DCM) was investigated in an attempt to elucidate clinical variables predicting sudden death (SD). In the patients with HCM, 68% of cardiac deaths occurred suddenly and unexpectedly. Variables associated with an increased risk to SD were young age (less than 30 years), reduced fractional shortening (less than 35%) and elevated left ventricular end-diastolic pressure (greater than or equal to 20 mmHg). Eight of the 10 patients who died suddenly during or immediately after strenuous exercise were less than 30 years old, and the collapse tended to be associated with exercise-induced ST-depression. In contrast, SD occurring during mild activities, resting or sleep was mainly observed in those aged 30 years or more. Ventricular tachycardia was observed on electrocardiographic monitoring in 24% of those 30 years or more, while it was rare in those under 30 years (5%). On the other hand, no SD was found in patients with apical hypertrophy nor in those 50 years or more. These observations suggest that HCM patients at a young age, with impaired left ventricular systolic and diastolic function, have an increased risk to SD. Since exercise-induced myocardial ischemia rather than ventricular arrhythmias appears to be the more likely mechanism for SD for those under 30 years old, restriction of strenuous exercise should be strongly advised for these patients. For those aged from 30 to 50 years, ventricular tachycardia should be controlled by antiarrhythmic agents for the prevention of SD. In patients with DCM, 24% of all cardiac deaths were attributed to SD. Although no variables reliably predicted SD, it was of note that only one patient out of 26 with SV1 + RV5 greater than or equal to 35 mm died suddenly. Whereas ventricular arrhythmias are known to be a contributing cause for SD, the prognostic significance of ventricular tachycardia on electrocardiographic monitoring in predicting SD has not yet been established. In addition, antiarrhythmic agents often precipitate hemodynamic deterioration. It therefore appears that use of antiarrhythmic agents is not a therapy of first choice and that primary treatment should be focused upon improvement in ventricular function in order to prevent SD in patients with DCM.
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PMID:Sudden death in hypertrophic and dilated cardiomyopathy. 263 25

OPC-8212, a newly synthesized noncatecholamine, nonglycosidic, orally effective inotropic agent, has been shown to exert a potent cardiotonic action in acute administration to patients with heart failure. However, its long-term effect has not yet been established. Eight patients with dilated cardiomyopathy (New York Heart Association functional class II-III) were given a single dose of 60 mg of OPC-8212 daily for 4 to 8 weeks. OPC-8212 produced symptomatic improvement in four patients. Though there were no detectable changes in arterial pressure and left ventricular end-diastolic dimension, heart rate and end-systolic dimension significantly decreased after administration of OPC-8212. Baseline fractional shortening rose significantly and depression of shortening in response to acute pressor stress (afterload mismatch) was corrected after OPC-8212. The end-systolic pressure-dimension relation was shifted to the left with a steeper slope. These findings indicate that the inotropic state was substantially enhanced by the drug. No adverse effects were observed in any patient. Thus, the drug appears to hold promise for the chronic treatment of patients with moderate congestive heart failure who are essentially asymptomatic at rest, but develop severe impairment of cardiac function in a stressed state.
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PMID:Sustained inotropic effects of a new cardiotonic agent. OPC-8212 in patients with chronic heart failure. 264 27

The effects of acute intravenous administration of ICI 118,587 (Corwin), a partial beta 1 agonist, were studied in nine patients with dilated cardiomyopathy and symptomatic congestive heart failure. Hemodynamic and metabolic parameters were measured using Swan-Ganz, arterial, and coronary sinus catheters. Repeated doses of Corwin produced no significant change in left ventricular performance, while a trend towards decreased blood pressure and stroke work was seen. No change occurred in coronary sinus blood flow, transmyocardial lactate extraction, or catecholamine release. One patient had significant depression of left ventricular function with hypotension. Thus, acute infusion of Corwin produced no beneficial inotropic responses, but rather produced features suggestive of further myocardial depression.
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PMID:Acute hemodynamic and metabolic effects of ICI 118,587 (Corwin), a selective partial beta 1 agonist, in patients with dilated cardiomyopathy. 286 73

The effects on left ventricular function and myocardial metabolism of Corwin (ICI 118,587), a selective beta-1 partial agonist, were evaluated in 12 patients with dilated cardiomyopathy. All patients were in sinus rhythm at the time of cardiac catheterization. Immediately before and 20 minutes after intravenous administration of 0.2 mg/kg Corwin over 2 minutes, high-fidelity left ventricular pressures and thermodilution coronary sinus blood flow were recorded along with ventriculograms in the 30 degrees right anterior oblique projection. In 11 patients, Corwin resulted in no change in heart rate, a fall in left ventricular end-diastolic pressure, a rise in left ventricular systolic pressure and an increase in cardiac index. There was a rise in both peak positive and peak negative dP/dt. End-diastolic and end-systolic volume indices fell, and ejection fraction rose. There was an increase in coronary sinus blood flow and a small rise in myocardial oxygen consumption. In contrast to these results in the group as a whole, in one patient Corwin produced depression of both systolic and diastolic left ventricular function. We conclude that, in many patients with dilated cardiomyopathy, Corwin produces an improvement in systolic and diastolic left ventricular function while at the same time only slightly increasing myocardial oxygen demand. In some patients, however, Corwin may result in a significant worsening of left ventricular performance due to its antagonistic effects.
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PMID:[Acute effect of the cardioselective beta-1-partial agonist, Corwin, on ventricular function and myocardial oxygen consumption in patients with dilated cardiomyopathy]. 287 68

In vivo and in vitro tests of cellular immunity were studied in patients with congestive cardiomyopathy to determine whether these patients have normal or depressed cell mediated immunity to common environmental antigens and mitogens. No abnormality was found, but this does not exclude the possibility that transient depression of cell mediated mechanisms occurs early in the illness before clinical presentation.
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PMID:Cellular immunity in congestive cardiomyopathy. The normal cellular immune response. 315 95

Previous reports have shown that increases in heart rate may result in enhanced left ventricular (LV) systolic and diastolic performance. To assess whether this phenomenon occurs in the presence of depressed LV function, the effects of pacing on LV pressure and volume were compared in seven patients with dilated cardiomyopathy (LV ejection fraction 0.19 +/- 0.11) and six patients with no or minimal coronary artery disease (LV ejection fraction 0.69 +/- 0.11). Patients with normal LV function demonstrated significant increases in LV peak-positive dP/dt, LV end-systolic pressure-volume ratio, LV peak filling rate, and a progressive leftward and downward shift of their pressure-volume diagrams, compatible with increased contractility and distensibility in response to pacing tachycardia. There was no change in LV peak-negative dP/dt or tau. Patients with dilated cardiomyopathy, in contrast, demonstrated no increase in either LV peak-positive dP/dt or the end-systolic pressure-volume ratio, and absence of a progressive leftward shift of their pressure-volume diagrams. Moreover, cardiomyopathy patients demonstrated no increase in LV peak-negative dP/dt or LV peak filling rate and a blunted downward shift of the diastolic limb of their pressure-volume diagrams. Tau, as determined from a derivative method, became abbreviated although never reaching control values. We conclude that patients with dilated cardiomyopathy may demonstrate little or no significant enhancement in systolic and diastolic function during atrial pacing tachycardia, suggesting a depression of both inotropic and lusitropic reserve.
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PMID:Depression of systolic and diastolic myocardial reserve during atrial pacing tachycardia in patients with dilated cardiomyopathy. 318 60

Ventricular aneurysms are rarely observed in viral myocarditis. Three cases whose left ventriculograms showed localized left ventricular aneurysms in the chronic phase of myocarditis are reported. The etiology in one case was herpes simplex virus (Case 1). Two cases (Case 2, 3) of myocarditis were admitted to our Coronary Care Unit in the acute phase, when diffuse hypokinesis of the left ventricle was demonstrated by two-dimensional (2-D) echocardiography. Hypokineses progressed to localized left ventricular aneurysm formation, demonstrated by cine angiography. In the acute phase, ST segment elevation was observed in these two cases, but it resolved. Abnormal Q waves also resolved in the chronic phase. Negative T waves were nearly normalized in one of them (Case 3). Abnormal Q waves with ST segment depression were observed in another case (Case 1). Thus, there were no characteristic or consistent findings suggesting a left ventricular aneurysm on electrocardiography. 2-D echocardiography and cine angiography proved useful for diagnosing this uncommon complication. Long-term follow-up of these cases will be important, because viral myocarditis can develop into dilated cardiomyopathy. The mechanism of left ventricular aneurysm following acute viral myocarditis included: (1) direct viral injury of the myocardium, (2) localized injury due to immunological mechanisms, and (3) coronary thrombosis due to increased platelet aggregation by viral infection.
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PMID:[Acute myocarditis with localized left ventricular aneurysm: a report of three cases]. 324 76

Prevention of sudden arrhythmic cardiac death must be preceded by identification of the high-risk patient to whom appropriate therapy can be given. The most common disease state associated with sudden cardiac death is coronary artery disease. Factors which identify a high-risk subset include: left ventricular dysfunction; frequent and complex arrhythmias on Holter monitoring; abnormal signal-averaged electrocardiograms; angina, ST depression, and exertional hypotension or ventricular arrthythmias on exercise testing; inducible sustained arrhythmias at electrophysiologic testing, or a combination of these factors. Other conditions which are known to be associated with sudden death include: dilated or congestive cardiomyopathy, hypertrophic cardiomyopathy, mitral valve prolapse, valvular heart disease, Wolff-Parkinson-White syndrome, myocarditis, congenital heart disease, electrolyte abnormalities, long QT syndromes, proarrhythmic effects of drugs, and less common conditions such as myocardial tumors and pulmonary hypertension. If the primary abnormality responsible for the tendency toward arrhythmias cannot be corrected, appropriate therapy should be administered to attempt to reduce the patient's risk of sudden arrhythmic cardiac death.
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PMID:Definition of patients at high risk of sudden arrhythmic cardiac death. 327 Nov 94


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