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

In heart failure, many alterations occur in the ventricle as a whole, as well as in the myocardial cell. In the first part of this review we report on the macroscopic structure of the left ventricle by analysing the relation between left ventricular dilatation and left ventricular hypertrophy in terms of ventricular wall stress. Peak systolic stress in dilated ventricles of patients with compensated heart failure does not differ from values obtained in normal ventricles, whereas the systolic stress-time integral is increased by more than 40%. The stress-time integral is a major determinant of myocardial oxygen consumption, and its reduction by peripheral vasodilation leads to a proportional decrease in left ventricular oxygen consumption. In contrast, the phosphodiesterase inhibitor, enoximone, decreases the stress-time integral without a proportional decrease in myocardial oxygen consumption, due to the competition between positive inotropic effect with increased oxygen consumption and a vasodilating effect with decreased oxygen consumption. Beta-1 adrenoceptor agonists increase myocardial oxygen consumption. In the second part of this review we report on the functional alterations of the following subcellular and molecular structures in the failing myocardium: (1) adrenoceptors and G-proteins; (2) sarcoplasmic reticulum with an altered force-frequency relationship; (3) the acto-myosin system with decreased velocity of shortening and increased economy of force generation. On the basis of these alterations, a disadvantageous chain of events develops in the failing myocardial cell.
 ...
PMID:The heart in heart failure. Ventricular and myocardial alterations. 183 95

Mechanical ventilation is a valuable therapeutic option in left ventricular failure because of its effect on ventricular load. However, weaning cardiac patients form mechanical ventilation may result in severe pulmonary oedema, especially if it is not properly prepared. Some of the factors which contribute to pulmonary oedema are: 1) increased venous return due to the inversion ot the regime of inthrathoracic pressures and the release of catecholamines commonly observed during weaning, 2) reduction of left ventricular compliance due to myocardial ischemia, compression of the cardiac chambers by the lungs, ventricular interdependence in some cases and left ventricular dilatation in others, 3) increased left ventricular afterload due to negative intrathoracic pressures and increased systolic blood pressure. Of all the causes of unsuccessful weaning, left ventricular dysfunction should be carefully considered because its treatment alone may enable the patients to be taken off the ventilator. The authors report six cases of pulmonary oedema in coronary patients after discontinuing mechanical ventilation. The administration I.V. enoximone, a phosphodiesterase inhibitor, prevented acute left ventricular dysfunction in 5 of the 6 cases and enabled successful and definitive weaning from mechanical ventilation.
 ...
PMID:[Left ventricular dysfunction while weaning from mechanical ventilation. Contribution of enoximone]. 214 40

The principle functions of the heart are to accept blood from the systemic and the pulmonary circulatory system, pump and deliver it to the whole body tissues and lungs. The term "heart failure" is used to describe the pathophysiological state in which an abnormality of cardiac function is responsible for failure of the heart to pump blood at a rate commensurate with the requirements of the metabolizing tissues, or to do so only from an elevated filling pressure. Thus, for a long period, heart failure has been thought of as a mechanical disorder of the heart and vessels, and its treatment has been based on improving impaired cardiac function and hemodynamic disorder. Recently multi-center, randomized placebo-controlled survival trials revealed that pure inotropic agents such as phosphodiesterase inhibitors succeeded in mechanical improvement, yet not only failed to prolong the patient's life, but also increased mortality. A number of neurohumoral mechanisms, which are activated in heart failure, were thought to be compensatory ones. However, survival trials demonstrated that two types of drug interfering with the renin-angiotensin system and the sympathetic nervous system reduced mortality. Those drugs are angiotensin-converting enzyme (ACE) inhibitors and beta blockers. ACE inhibitors reduce the direct effects of angiotensin II on myocardial cells, which may lead to cell necrosis, imbalanced remodeling through fibrosis, and attenuate the progressive ventricular dilatation. Local tissue renin-angiotensin system may be potentially important in regulating the angiotensin II production in both heart and vessels.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Pathophysiology and treatment of congestive heart failure--recently advanced strategy for heart failure]. 774 73

We report a 29-year-old primigravid who developed cardiac failure following postpartum haemorrhage unresponsive to volume resuscitation and therapy with catecholamines and phosphodiesterase-inhibitors. Transoesophageal echocardiography (TEE) demonstrated left atrial and ventricular dilatation and global left ventricular hypokinesis. No elevation of serum MB-isoenzyme fraction was detected and other organ functions remained stable. Although emergency cardiac transplantation was considered in the presented patient, the institution of intra-aortic counterpulsation was decided on as a first treatment option. Intra-aortic balloon counter-pulsation rapidly improved cardiac function and led to weaning from pharmacological cardiac support within a few days. Mechanical circulatory assist devices can be life-saving in postpartum-haemorrhage-associated cardiac failure.
 ...
PMID:Successful treatment of severe myocardial failure after postpartum haemorrhage with the use of an intra-aortic balloon pump. 1019 53

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.
 ...
PMID:New surgical options for the failing heart. 1051 85

Pulmonary hypertension is characterized by a progressive increase in pulmonary arterial pressure in association with dilatation and hypertrophy of the right ventricle, causing gradual reduction in ejection fraction. The increase in mean pulmonary arterial pressure may be passive, due to increased downstream pressure, hyperkinetic due to increased cardiac output, or due to increased pulmonary vascular resistance resulting from changes in the pulmonary vessels. In an advanced stage of pulmonary hypertension there may be right ventricular dilatation and hypertrophy, tricuspid regurgitation and septal deviation, with consequent effects on cardiac function. Clinical symptoms are not specific. Until recently, the treatment of pulmonary hypertension was limited to anticoagulation, supplementary oxygen and high-dose calcium channel blockers, in association with diuretics and digoxin where indicated. Recently approved treatments are nitric oxide, sildenafil--a phosphodiesterase-5 inhibitor, analogs of prostacyclin, and nonselective and selective endothelin receptor inhibitors. Surgery and anaesthesia pose a significant risk for patients with pulmonary hypertension. Right ventricular failure, persistent postoperative hypoxia and coronary ischaemia are among the potential postoperative complications.
 ...
PMID:[Pulmonary hypertension]. 1951 79