Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 79-year-old female was admitted to our hospital because of a malignant pleural effusion following mastectomy 4 years ago. In the patient's history arterial hypertension and previous inferior myocardial infarction have been known. Two doses of 20 mg mitoxantrone were installed intrapleurally at an interval of 4 weeks. Six hours after the second mitoxantrone application and the patient had increasing dyspnea with consecutive left heart failure, pulmonary congestion, and a drop of blood pressure. The white-cell count was 14800/mm3. The levels of creatinine phosphokinase (CPK), lactate dehydrogenase (LDH) and serum aspartate aminotransferase (SGOT) were in the normal range. Transthoracic echocardiography showed concentric left ventricular hypertrophy and a markedly decreased fractional shortening, but no left ventricular dilatation. The electrocardiogram showed newly appeared down-sloping ST-segments and inverted T-waves. Clinical recovery was achieved after 6 days by application of oxygen, dobutamine and furosemide followed by angiotensin converting enzyme inhibition and digitalis. In the echocardiographic control examination 14 days later left ventricular function had normalized. The changes of electrocardiogram normalized 4 weeks later.
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PMID:[Mitoxantrone-induced acute left heart failure after intrapleural administration]. 937 56

In addition to being accepted therapy in hypertension and heart failure, ACE inhibitors may well offer a new dimension in anti-ischaemic therapy. Currently, anti-ischaemic properties have been demonstrated by ACE inhibitors in selected patient groups, including patients with left ventricular dysfunction with or without a direct temporal relationship with myocardial infarction. Anti-ischaemic effects of ACE inhibitors become apparent late after initiation of treatment and suggest a structural rather than a functional effect. Underlying mechanisms may include a reduction in ventricular dilatation and (abnormal) cardiac hypertrophy, leading to less myocardial oxygen demand and, possibly, improved subendocardial blood supply, and vasculoprotective effects, i.e. anti-atherosclerotic and antiremodelling properties, a beneficial effect on the fibrinolytic system and an improvement in abnormal endothelial vasodilator function. The latter aspect is most probably the pivotal mode of action where the anti-ischaemic profile of ACE inhibition is concerned. An improvement in endothelial dysfunction has been shown in patients with mild to moderate coronary artery disease [Trial on Reversing ENdothelial Dysfunction (TREND)]. It is of importance that, in both clinical experiments and human studies, the role of bradykinin appears central in the structural and functional cardiovascular effects of ACE inhibition. This is particularly true for the improvement of impaired endothelial function. Myocardial ischaemia evokes vasoconstrictor neurohormonal activation, which may lead to coronary vasoconstriction in diseased coronary segments. The subsequent abnormal endothelial function leads to diminished coronary flow and also increases systemic vasotone and afterload, thus unfavourably altering the myocardial oxygen supply/demand ratio. Under laboratory conditions, acute ACE inhibition counteracts this activation in humans. However, it is speculated that this anti-ischaemic mechanism may become operative and clinically important during long term oral ACE inhibitor therapy when endothelial function improves, and may subsequently protect against the vasoconstrictor effect of neurohormonal activation. As it is unlikely that the mechanisms mentioned above are only relevant in patients with ventricular dysfunction or heart failure, several large controlled trials are currently examining the long term anti-ischaemic and cardiovascular protective effects of ACE inhibition in patients at risk of a cardiovascular event [Heart Outcomes Prevention Evaluation study (HOPE)], with a normal cardiac function [Prevention of Events with ACE inhibition study (PEACE)] or in all patients with coronary artery disease irrespective of cardiac function [EUropean trial of Reduction Of cardiac events with Perindopril in stable coronary Artery disease (EUROPA)].
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PMID:Bradykinin-mediated cardiovascular protective actions of ACE inhibitors. A new dimension in anti-ischaemic therapy? 942 46

Temporal and spectral analysis of heart rate variability over 24 hours (HRV) was undertaken in 89 patients with primary dilated cardiomyopathy (DCM) confirmed by left ventriculography with normal coronary angiography and compared with 60 control subjects. The left ventricular ejection fraction was 35 +/- 12% in the DCM patients (71 men and 18 women: age 51 +/- 11 years). Clinical signs of cardiac failure were observed in 66% of patients, requiring medication in 62% of patients (diuretics: 47%, digitalis: 45% and ACE inhibitors: 33%). The HRV was significantly lower in the DCM patients than in the control group, even in the absence of clinical signs of cardiac failure. The global HRV was correlated to left ventricular fractional shortening (r = 0.5, p < 0.001) and peak oxygen consumption on exercise (r = 0.56, p < 0.01), but was independent of the degree of left ventricular dilatation, pulmonary capillary pressure and cardiac index. It was not significantly different in cases of sustained or non-sustained ventricular tachycardia on Holter ECG or in cases with late ventricular potentials on signal averaging of the surface ECG. During follow-up of 51 +/- 35 months, patients with decreased HRV on the global indices and those reflecting sympathetic activity had a much higher risk of cardiovascular death and of cardiac transplantation (p < 0.01). The authors conclude that HRV is decreased in DCM. This is mainly related to the degree of left ventricular dysfunction and is independent of the ventricular arrhythmogenic substrate. The HRV may also identify subgroups of patients with DCM at high risk of cardiovascular death or of haemodynamic decompensation requiring cardiac transplantation.
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PMID:[Temporal and spectral analysis of heart rate variability in primary dilate cardiomyopathy: evaluation by case control study]. 974 48

Vasodilator therapy with nitrates has been used for almost a century to bring relief to patients suffering from angina. The acute anti-ischemic effects of nitro-vasodilators for the treatment and prevention of anginal attacks is unquestioned. In addition, nitrates are administered in order to reduce symptomatic and silent ischemic episodes, in patients with proven coronary heart disease who exert ST segment alterations on Holter monitoring. The reduction in total ischemic burden may result in an improved prognosis with regard to infarct prevention and possible prevention of deterioration of left ventricular function due to repetitive episodes of myocardial ischemia. In patients with unstable angina, administration of nitrates significantly diminishes ischemic episodes and reduces the number of clinically symptomatic anginal attacks. The prevention of left ventricular dilatation in patients within the first few days and months following acute myocardial infarction may be due to the reduced preload. In patients with heart failure, preload reduction with nitrates and afterload reduction with hydralazine was tested versus angiotensin converting enzyme (ACE) inhibitors. However, unfortunately, very few data are available concerning the combination therapy of ACE inhibitors and nitrates in heart failure and following acute myocardial infarction. Long-term continuous administration of high doses of nitrates may cause nitrate tolerance, thus reducing the vasodilator potency of these drugs. Since nitrates were introduced into medical therapy many decades before randomized controlled trials were performed, and evidence-based medicine became the basic principal for medical therapy, there are still indications and situations where the full therapeutic potential of nitrates is not being fully appreciated. During recent decades, other anti-ischemic drugs, i.e., beta-receptor agonists and calcium channel blockers, were introduced into the clinical setting and contributed to an optimized therapy for patients with coronary heart disease. Nevertheless, due to their proven and unsurmounted symptomatic efficacy, nitrates will remain one of the cornerstones of acute and long-term therapy of patients with coronary heart disease far beyond the year 2000.
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PMID:Role of nitrates for the therapy of coronary artery disease patients in the years beyond 2000. 1049 56

Heart failure is common in patients aged over 65 years, and is the fourth leading cause of hospitalization in the United States. Treatment of congestive heart failure involves remodeling the cardiac chamber with ventricular dilatation. New approaches to resolve this problem include medical therapies (digoxin, diuretics, ACE inhibitors, beta-blockers and phosphodiesterase inhibitors) to stabilize patients, followed by chamber remodeling. As yet, surgical intervention in advanced heart failure has been contraindicated, but newly evolving strategies show significant promise. It appears possible that patients can receive surgical therapy to improve cardiac function, followed by state-of-the-art medical therapy for congestive heart failure. This combined medical/surgical approach has led to the evolution of a new subspecialty within cardiology that deals with the management of heart failure.
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PMID:New surgical options for the failing heart. 1051 85

Clinical findings in fifteen dogs with tricuspid valve dysplasia are described. Thirteen dogs had loud systolic heart murmurs. Eleven of them hat a palpable precordial thrill over the same location. In 14 dogs, right heart enlargement was suspected on thoracic radiographs and electrocardiography. Right atrial dilation was seen echocardiographically in all dogs. Fourteen dogs had additional right ventricular dilatation, some with hypertrophy as well. Doppler echocardiography revealed tricuspid valve regurgitation. Seven dogs remained free of clinical symptoms to date. If symptoms of decompensation develop with tricuspid dysplasia, diuretics, ACE inhibitors and eventually positive inotrope drugs are indicated. Antiarrhythmic drugs may become necessary in cases of supraventricular tachyarrhythmias.
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PMID:[Tricuspid valve dysplasia in fifteen dogs]. 1085 Jan 63

Congestive heart failure is a multiple aetiology, high prevalence, poor prognosis cardiovascular disorder. Medical treatment of dilated cardiomyopathy is aimed at alleviating the symptoms of heart failure. Diuretics, ACE inhibitors and very recently, beta-blockers have been shown to have favourable effects on symptoms, exercise capacity and mortality. Growth hormone (GH) and insulin-like growth factor (IGF)-1 are involved in several physiological processes such as the control of muscle mass and function, body composition and regulation of nutrient metabolism. The roles of GH and IGF-1 as modulators of myocardial structure and function are well established. Receptors for both GH and IGF-1 are expressed by cardiac myocytes; therefore, GH may act directly on the heart or via the induction of local or systemic IGF-1, whereas IGF-1 may act by endocrine, paracrine or autocrine mechanisms. Patients with acromegaly have an increased propensity to develop ventricular hypertrophy and cardiovascular diseases and, in addition, an impaired cardiac efficiency is observed in patients with GH deficiency. Animal models of pressure and volume overload have demonstrated up-regulation of cardiac IGF-1 production and expression of GH and IGF-1 receptors, implying that the local regulation of these factors is influenced by haemodynamic changes. Moreover, experimental studies suggest that GH and IGF-1 have stimulatory effects on myocardial contractility, possibly mediated by changes in intracellular calcium handling. Heart failure is caused by ventricular dilatation with abnormal wall thickening, which leads to impaired cardiac performance; therefore, based on the evidence available for GH we would expect beneficial effects from the use of GH in these patients. Several papers highlight the positive influence of GH in the regulation of heart development and performance. In patients with GH deficiency, GH administration dramatically improves cardiac function. In small nonblind studies, both short and long term GH treatment have demonstrated beneficial effects in patients with heart failure secondary to ischaemic or idiophatic cardiomyopathy. Recently, two randomised, placebo-controlled studies, did not show significant GH-mediated improvement in cardiac performance in patients with dilated cardiomyopathy, despite significant increases in IGF-1. Acquired GH resistance, might be an important feature of severe heart failure and explain the different responses to GH therapy seen in different patients. Whether GH treatment will finally find a place, and with which modalities, in the treatment of heart failure remains to be established.
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PMID:Role of growth hormone in chronic heart failure. Therapeutic implications. 1108 97

Left ventricular remodeling is the process by which ventricular size, shape, and function are regulated by mechanical, neurohormonal, and genetic factors. Remodeling may be physiological and adaptive during normal growth or pathological due to myocardial infarction, cardiomyopathy, hypertension, or valvular heart disease. Postinfarction remodeling has been divided into an early phase within 72 hours and a late phase beyond 72 hours. The early phase involves expansion of the infarct zone, which may result in early ventricular rupture or aneurysm formation. Late remodeling involves the left ventricle globally and is associated with time-dependent dilatation, the distortion of ventricular shape, and mural hypertrophy. Hypertrophy and collagen degradation are adaptive responses during postinfarction remodeling. Myocardial repair is triggered by cytokines released from injured myocytes. Ventricular remodeling is influenced most by infarct artery patency. Once infarct evolution has occurred, pharmacological intervention, like ACE inhibition and beta-adrenoreceptor blocking agents, may minimize infarct expansion and ventricular dilatation and improve the long-term prognosis.
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PMID:[Pathophysiology and therapeutic aspects of left ventricular "remodeling" in the post-infarct phase]. 1177 72

Therapy for heart failure has traditionally been directed to such short-term functional abnormalities as low cardiac output, high filling pressures, and fluid retention. More recently, it has become clear that therapy must also inhibit the proliferative responses that contribute to the progressive deterioration of the failing heart. That heart failure is more than a hemodynamic disorder became apparent when clinical trials showed that drugs that improve such functional abnormalities as high venous pressure and low cardiac output failed to improve long-term prognosis. Most vasodilators, in spite of alleviating short-term problems caused by excessive afterload, increase long-term mortality; the notable exceptions are ACE inhibitors, the ability of which to prolong survival and inhibit remodeling can be attributed to inhibition of proliferative signaling. Other clinical trials showed that inotropic drugs, while providing immediate relief of symptoms, generally shorten long-term survival, whereas beta-adrenergic receptor blockers, which inhibit proliferative signaling by norepinephrine, improve prognosis. These findings can be explained by crossovers between functional and proliferative signaling, among the most important of which is the ability of neurohumoral mediators, such as norepinephrine and angiotensin II, to stimulate maladaptive hypertrophy, remodeling, apoptosis and other deleterious proliferative responses in the failing heart. The emerging understanding of the role of cytoskeletal and cell adhesion molecules in activating maladaptive proliferative responses suggests additional targets for therapy, and the rapid pace of discovery in molecular biology promises additional opportunities to inhibit this abnormal signaling, which causes progressive ventricular dilatation (remodeling) and cardiac cell death, now recognized to be major problems in this syndrome.
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PMID:Proliferative signaling and disease progression in heart failure. 1192 68

The effect of ACE inhibition after myocardial infarction (MI) on MI healing and remodeling in the presence of hypertension is not exactly known. Therefore, the effect of quinapril on scar formation, remodeling and hemodynamics was studied in spontaneously hypertensive rats (SHR). Nine weeks after moderate and large MI, left ventricular end-diastolic pressure (LVEDP) and passive pressure-volume relations were similar in 28-week-old hypertensive and normotensive rats. Chronic therapy with quinapril (6 mg/kg/day, started 30 min post-MI) reduced LVEDP and LV to body weight ratio, yet did not affect pressure-volume relations. Quinapril increased MI size and reduced the content and brightness of collagen fibers in the scar examined by polarized light microscopy. In conclusion, ventricular dilatation after MI was not accelerated in SHR, probably due to LV hypertrophy. Quinapril produced beneficial hemodynamic effects similar to that observed in the normotensive rat model. The significance and timing of ACE inhibitor-induced impairment of scar formation need further evaluation.
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PMID:Ventricular remodeling after myocardial infarction and effects of ACE inhibition on hemodynamics and scar formation in SHR. 1193 99


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