cardiovascular-agents and Ventricular-Dysfunction

Topics: Aged; Cardiomegaly; Cardiovascular Agents; Echocardiography; Female; Heart Failure; Humans; Hypertension; Practice Guidelines as Topic; Stroke Volume; Ventricular Dysfunction

Topics: Cardiac Surgical Procedures; Cardiovascular Agents; Chronic Disease; Heart Failure; Humans; Prevalence; Risk Factors; Stroke Volume; Systole; United States; Ventricular Dysfunction

The clinical relevance of diastolic dysfunction in heart failure has recently been emphasized. In fact, the presence of signs of heart failure does not imply a depressed left ventricular systolic function; moreover, the severity of heart failure and effort tolerance are more closely related to diastolic than to systolic indexes. However, the principal trials about the treatment of heart failure were mainly addressed to patients with significant left ventricular systolic dysfunction, whereas the optimal therapy for diastolic dysfunction is not well known. The aim of this review was to assess the rationale and the therapeutic options in heart failure due to diastolic dysfunction. A diastolic dysfunction can be exclusive or associated with systolic dysfunction, as in dilated cardiomyopathy. It has to be noted that in this disease an improvement of diastolic function was demonstrated for most of the drugs currently employed in the treatment of heart failure, such as vasodilators, ACE inhibitors, beta-blockers, digitalis, and other inotropic drugs. Moreover, the favorable effect of the treatment on diastolic parameters (reduction of left ventricular filling pressure, regression of restrictive filling pattern) is associated with a positive prognostic impact. The main objective of the treatment of heart failure with preserved left ventricular systolic function is to control the symptoms by means of lowering high left ventricular filling pressure without significantly lowering cardiac output. According to the therapeutic guidelines of the American College of Cardiology/American Heart Association Task Force, the drugs indicated to treat symptomatic patients with heart failure and preserved left ventricular systolic function are diuretics and nitrates. Potentially useful, but with insufficiently proven efficacy are beta-blockers, calcium antagonists and ACE inhibitors, whereas direct vasodilators and inotropic drugs were considered inadvisable. It is important to remember that the treatment might possibly be oriented to the cause and also to the possible precipitating factors of the heart failure syndrome (i.e. ischemia, tachycardia, arrhythmias, hypertension). In conclusion, considering the relatively common incidence of heart failure due to prevalent diastolic dysfunction, and the few available data about the therapeutic options in these patients, large multicenter trials devoted to the treatment of this syndrome are needed.

Topics: Cardiovascular Agents; Diastole; Heart Failure; Humans; Systole; Ventricular Dysfunction

To review the incidence, pathophysiology, significance, diagnosis, and treatment of heart failure with normal systolic function in older patients.. Scientific reports of diastolic ventricular dysfunction in both the general population and the geriatric population were identified from repeated searches of the MEDLINE database and citations from appropriate articles.. Studies were included only if they demonstrated proper methodology, were from a reputable source, and were published in a peer-reviewed journal.. Relevant data were obtained from the articles, with special importance placed on studies designed to examine older patients exclusively or as part of a subgroup in a larger study. Emphasis was placed on data pertaining to the pathophysiology, prognosis, and diagnosis of patients with diastolic dysfunction compared with normals and patients with systolic dysfunction as an etiology of heart failure. Therapeutic interventions were selected for the presence of prospective data with concrete end points such as mortality, functional class, exercise capacity, and regression of left ventricular hypertrophy.. Diastolic ventricular dysfunction is a significant problem in older people, with at least 40% of older heart failure patients having diastolic dysfunction as the etiology of their heart failure. The pathophysiology of diastolic dysfunction is varied but usually involves impaired left ventricular relaxation and/or increased ventricular stiffness, each partially related to normal aging changes, as well as underlying cardiovascular diseases. The significance of heart failure caused by diastolic dysfunction is great, with increased morbidity and mortality compared with other cardiac diseases that have the same preserved systolic function. Diagnosis of diastolic dysfunction can be clinically difficult and often requires further testing to determine if diastolic dysfunction is present. At this time, no therapy specifically treats diastolic dysfunction, but several medications, such as diuretics, calcium channel blockers, beta blockers, and angiotension-converting enzyme inhibitors, offer symptomatic relief and may prevent progression of the disorder.

Topics: Aging; Animals; Cardiovascular Agents; Diastole; Geriatrics; Heart Failure; Humans; Systole; Ventricular Dysfunction

Right ventricular (RV) dysfunction following left ventricular (LV) failure is associated with poor prognosis. RV remodeling is thought initiated by the increase in the afterload of RV due to secondary pulmonary hypertension (PH) to impaired LV function; however, RV molecular changes might occur in earlier stages of the disease. cGMP (cyclic guanosine monophosphate)-phosphodiesterase 5 (PDE5) inhibitors, widely used to treat PH through their pulmonary vasorelaxation properties, have shown direct cardiac benefits, but their impacts on the RV in LV diseases are not fully determined. Here we show that RV molecular alterations occur early in the absence of RV hemodynamic changes during LV pressure-overload and are ameliorated by PDE5 inhibition. Two-day moderate LV pressure-overload (transverse aortic constriction) neither altered RV pressure/ function nor RV weight in mice, while it induced only mild LV hypertrophy. Importantly, pathological molecular features were already induced in the RV free wall myocardium, including up-regulation of gene markers for hypertrophy and inflammation, and activation of extracellular signal-regulated kinase (ERK) and calcineurin. Concomitant PDE5 inhibition (sildenafil) prevented induction of such pathological genes and activation of ERK and calcineurin in the RV as well as in the LV. Importantly, dexamethasone also prevented these RV molecular changes, similarly to sildenafil treatment. These results suggest the contributory role of inflammation to the early pathological interventricular interaction between RV and LV. The current study provides the first evidence for the novel early molecular cross-talk between RV and LV, preceding RV hemodynamic changes in LV disease, and supports the therapeutic strategy of enhancing cGMP signaling pathway to treat heart diseases.

Topics: Animals; Calcineurin; Cardiomegaly; Cardiovascular Agents; Dexamethasone; Disease Models, Animal; Extracellular Signal-Regulated MAP Kinases; Heart Ventricles; Hemodynamics; Macrophages; Male; Mice, Inbred C57BL; Phosphodiesterase 5 Inhibitors; Sildenafil Citrate; Ventricular Dysfunction; Ventricular Function, Left; Ventricular Function, Right; Ventricular Pressure

Topics: Angioplasty, Balloon, Coronary; Arrhythmias, Cardiac; Cardiovascular Agents; Clinical Trials as Topic; Emergency Medical Services; Health Promotion; Hospitalization; Humans; Myocardial Infarction; Risk Assessment; Thrombolytic Therapy; Time Factors; Ventricular Dysfunction