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)

The incidence of hypertrophic cardiomyopathy progressing to dilated cardiomyopathy is rare. A patient diagnosed at age 22 and followed for 24 years who progressed to a dilated cardiomyopathy with severe congestive heart failure is reported. Left ventricular dilatation in hypertrophic cardiomyopathy may be due to a complication of surgery, beta-blocker therapy, or myocardial infarction. It may also represent the natural history in a subset of patients with hypertrophic cardiomyopathy.
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PMID:Progression from hypertrophic cardiomyopathy to dilated cardiomyopathy. 239 73

Thallium-dipyridamole imaging is a very sensitive test for predicting cardiac events after noncardiac surgery, but it lacks specificity. To improve specificity, a semiquantitative scoring system was developed that combined dipyridamole-induced reversible left ventricular dilatation with scintigraphic indexes for severity and extent of reversible perfusion defects. Using this scoring system, patients were classified into low, intermediate and high risk subgroups. Thallium-dipyridamole imaging was performed in 66 patients before major general and vascular surgery. Thirty-nine patients classified as low risk (30 with normal scans and 9 with fixed defects) underwent surgery uneventfully. Surgery was cancelled in 6 patients with extensive thallium redistribution and coronary angiography was performed because of severe coronary artery disease in 5 and idiopathic dilated cardiomyopathy in 1. In the remaining 21 patients with thallium redistribution, a positive statistical correlation (p = 0.001) between scintigraphic indexes of severity and extent, and cardiac events was noted. Using cutoff values for the scintigraphic indexes, patients with reversible defects could be classified into intermediate and high risk subgroups. Only 1 of 11 patients at intermediate risk developed a complication, whereas 8 of 10 patients at high risk had a postoperative event (7 deaths and 1 myocardial infarction). Thus, using scintigraphic indexes for severity and extent, patients with reversible defects can be stratified into an intermediate risk subgroup that can safely undergo surgery and a high risk subgroup that requires coronary angiography.
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PMID:Usefulness of the severity and extent of reversible perfusion defects during thallium-dipyridamole imaging for cardiac risk assessment before noncardiac surgery. 275 71

Infarct expansion and infarct extension are events early in the course of myocardial infarction with serious short- and long-term consequences. Infarct expansion, disproportionate thinning, and dilatation of the infarct segment probably begin within hours of acute infarction and usually reach peak extent within seven to 14 days. Clinical data suggest that infarct expansion occurs in approximately 35% to 45% of anterior transmural myocardial infarctions and to a lesser extent in infarctions at other sites. Although expansion usually develops in large infarcts, the extent of transmural necrosis rather than absolute infarct size predicts its occurrence. Expansion has an adverse effect on infarct structure and function for several reasons. Functional infarct size is increased because of infarct segment lengthening, and expansion results in over-all ventricular dilatation. Thus, patients with expansion of an infarct have poorer exercise tolerance, more congestive heart failure symptoms, and greater early and late mortality than those without expansion. Infarct rupture and late aneurysm formation are two additional structural consequences of infarct expansion. Experimental and clinical data suggest that the incidence and severity of expansion can be modified by interventions. Increased ventricular loading conditions and steroidal and nonsteroidal antiinflammatory agents make expansion more severe. Reperfusion of the infarct segment and pharmacologic interventions that decrease ventricular afterload lessen the severity of expansion. Previous myocardial infarction and preexisting ventricular hypertrophy may also limit the development of infarct expansion. Infarct extension is defined clinically as early in-hospital reinfarction after a myocardial infarction. The pathologic finding of infarct extension is necrotic and healing myocardium of several different recent ages within the same vascular territory. Although this pathologic criterion usually cannot be verified, studies employing invasive and noninvasive assessment of patients with early reinfarction provide evidence that the new myocardial injury is usually in the same vascular risk region as the original infarction. A variety of different criteria have been applied in the clinical diagnosis of infarct extension, and this has resulted in a large range of estimated frequencies from under 10% to as high as 86%. High estimates are found in studies using one or two nonspecific criteria such as ST segment shift or reelevation of total CK. The lowest rates have been found when combinations of criteria are used.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Myocardial infarct expansion, infarct extension, and reinfarction: pathophysiologic concepts. 288 58

Increased ventricular volume is one of the most powerful predictors of reduced survival in patients with heart disease. Despite its well-documented prognostic significance, the magnitude of the progression of ventricular dilatation from the acute to the chronic phase of myocardial infarction has only recently been appreciated. In an experimental preparation of myocardial infarction in rats, left ventricular cavitary volume increased progressively even after histologic resolution of the infarct region. We hypothesized that this remodeling of the infarcted left ventricle was a response to an increase in both systolic and diastolic wall stresses and that captopril, by reducing wall stress, would attenuate the process. For comparably sized infarcts, the captopril-treated rats had smaller ventricular volumes at common distending pressures, yet they had maintained or improved cardiac output. Most importantly, long-term captopril therapy also prolonged the survival of these rats with experimental myocardial infarction. The implication of these animal studies is that the potential exists for the attenuation of progressive ventricular enlargement and improvement of survival of patients recovering from a myocardial infarction. At the present time, no information is available in patients as to the therapeutic potential of interrupting this insidious process of ventricular dilatation in order to improve survival. Clinical trials are required to determine whether salutary benefits similar to those observed in animals can be provided to patients recovering from a myocardial infarction.
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PMID:Ventricular enlargement and reduced survival after myocardial infarction. 295 70

We conducted a double-blind, placebo-controlled trial to determine whether ventricular dilatation continues during the late convalescent phase after myocardial infarction and whether therapy with captopril alters this process. Fifty-nine patients with a first anterior myocardial infarction and a radionuclide ejection fraction of 45 percent or less underwent cardiac catheterization 11 to 31 days after infarction, when they were not in overt congestive heart failure. They were randomly assigned to placebo or captopril and were followed for one year. A repeat catheterization was performed to evaluate interval changes in hemodynamic function and left ventricular volume. Thirty-eight male patients were evaluated with maximal-exercise treadmill tests every three months. No differences were detected at base line in clinical, hemodynamic, or quantitative ventriculographic variables. During one year of follow-up, the end-diastolic volume of the left ventricle increased by a mean [+/- SEM] of 21 +/- 8 ml (P less than 0.02) in the placebo group, but by only 10 +/- 6 ml (P not significant) in the captopril group. The left ventricular filling pressure remained elevated with placebo but decreased (P less than 0.01) with captopril. In a subset of 36 patients who were at high risk for ventricular enlargement because they had persistent occlusion of the left anterior descending coronary artery, captopril prevented further ventricular dilatation (P less than 0.05). Patients given captopril also had increased exercise capacity (P less than 0.05). This preliminary study indicates that after anterior myocardial infarction, ventricular enlargement is progressive and that captopril may attenuate this process, reduce filling pressures, and improve exercise tolerance.
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PMID:Effect of captopril on progressive ventricular dilatation after anterior myocardial infarction. 296 17

To evaluate pathologic features of myocardial infarction of the right ventricle (MI-RV), we analyzed 106 autopsy cases with transmural myocardial infarction (MI) (fresh in 46 cases and healed in 60). Anterior MI was observed in 47, posterior MI in 54 and lateral in 5. There were 13 cases (12%) with MI-RV (anterior in 1 case and posterior in 12), which included 10 cases with fresh MI and 3 with healed MI. All cases with MI-RV had associated transmural interventricular septal infarction. Of the 13 cases with MI-RV, 9 (69%) had right ventricular dilatation (RVD) and 2 had right ventricular hypertrophy. Extensive MI-RV (more than 1/3 of the right ventricle) was observed in 8 (89%) of those with RVD. Of 93 cases of MI without MI-RV, 14 (16%) had RVD. The incidence of RVD was greater in cases with MI-RV than in those without (p less than 0.005). All 12 cases with posterior MI-RV had significant (greater than or equal to 75%) narrowing of the right coronary artery (RCA), and 19 cases (87%) of those with posterior MI without MI-RV, had similar lesions. In conclusion, the incidence of RVD and significant narrowing of RCA was greater in cases with posterior MI-RV than in those with posterior MI.
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PMID:Pathologic study of myocardial infarction of the right ventricle. 296 27

This study determines the noninvasive prognostic predictors (using radionuclide angiography) in patients with severe left ventricular dysfunction (resting ejection fraction less than or equal to 35 percent) secondary to coronary artery disease. We retrospectively evaluated 94 such patients using rest and exercise radionuclide ventriculography. At a mean follow-up of 16 months, cardiac events occurred in 22 patients: ten patients died of cardiac causes, five patients sustained nonfatal myocardial infarction, and seven patients developed severe congestive heart failure (class 4). Results indicate that patients with severe left ventricular dysfunction may be stratified into different risk groups according to left ventricular size. Marked left ventricular dilatation identifies a subgroup at high risk.
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PMID:Left ventricular dilatation. Prognostic value in severe left ventricular dysfunction secondary to coronary artery disease. 299 Aug 23

Angiotensin converting enzyme (ACE) inhibitors are not known to have a direct effect on the myocardium. However, there is some evidence to suggest that they can play an important role in protecting the heart during the evolution of hypertensive and coronary arterial disease, both acutely and on a long term basis. Reduction of afterload by balanced arterial and venular dilatation has led to a sustained improvement of cardiac performance both in hypertension and heart failure. Reversal of cardiac hypertrophy has been shown to restore inotropic responsiveness to stimulators of the adenylate cyclase system. Following myocardial infarction, captopril has prevented undue ventricular dilatation and normalized left ventricular chamber stiffness; this prevented deterioration of cardiac function and improved long term survival after infarction. Control of secondary aldosteronism and prevention of hypokalaemia can play an important role in the prevention of cardiac arrhythmias. The lack of reflex sympathetic stimulation during long term captopril therapy can also play a favourable role in that respect. Although highly speculative, evidence is accumulating that ACE inhibition could have a cardioprotective effect in acute myocardial ischaemia. It is based on the demonstration that renin can be produced by myocardial cells, that angiotensin is liberated by the ischemic myocardium and that angiotensin in high renin conditions plays an active constrictor role in regulating the coronary circulation.
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PMID:Prospectives for angiotensin converting enzyme inhibition in heart diseases. 300 6

The prevention or attenuation of the development of heart failure by the angiotensin converting enzyme inhibitor captopril was examined in two animal models, spontaneously hypertensive rats and rats with myocardial infarction produced by coronary artery ligation. In 24-month-old female spontaneously hypertensive rats with marked left ventricular hypertrophy, cardiac output was reduced despite an increase in ventricular volume, resulting in a greatly reduced ejection fraction. Treatment with captopril from 14 to 24 months of age maintained forward output and prevented ventricular dilatation so that ejection fraction remained normal; left ventricular hypertrophy regressed to levels observed in six-month-old spontaneously hypertensive rats. In rats with moderate and large infarcts three months after ligation, left ventricular filling pressures were elevated, forward output was reduced, and ventricular volumes were greatly increased. Long-term therapy with captopril maintained filling pressures within normal limits and maintained forward output from a lesser dilated left ventricle to yield an ejection fraction that was elevated compared with that in untreated rats. Thus, the potentially deleterious remodeling of the left ventricle in heart failure, an extensive increase in mass and chamber volume, can be favorably altered by long-term angiotensin converting enzyme inhibition (captopril) with salutary effects on hemodynamics.
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PMID:Angiotensin converting enzyme inhibition and ventricular remodeling in heart failure. 306 98

Acute myocardial infarction is associated with complex neuroendocrine changes, including release of arginine vasopressin, norepinephrine, and epinephrine, and activation of the renin-angiotensin system. Arginine vasopressin levels are maximal on admission, and subsequently fall even in patients in whom left ventricular failure develops. Plasma levels of norepinephrine and epinephrine are at their highest on admission and return to the normal range in patients with uncomplicated infarction, but they remain significantly elevated in patients in whom left ventricular failure or late ventricular arrhythmias develop. In contrast to catecholamines and arginine vasopressin, plasma renin and angiotensin levels are within normal limits on admission in patients without complications but increase by the third day. Patients with left ventricular failure already have increased plasma levels of renin and angiotensin on admission, but further marked and persistent increases occur over the following days. All of the aforementioned hormones may interact to cause systemic or coronary vasoconstriction, which may have short-term adverse hemodynamic consequences. Furthermore, increased afterload may result in infarct expansion and left ventricular dilatation, which will impair left ventricular function still further. Interruption of the cycle of vasoconstriction and worsening left ventricular failure by angiotensin converting enzyme inhibitors may reduce the incidence of heart failure after myocardial infarction.
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PMID:Neuroendocrine changes in acute myocardial infarction. 306


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