Therapy For Chronic Congestive Heart Failure Research Articles

Management of Chronic Congestive Heart Failure Caused by Myxomatous Mitral Valve Disease in Dogs: A Narrative Review from 1970 to 2020.

Simple SummaryMyxomatous mitral valve disease (MMVD) is the most common acquired cardiovascular disease in dogs. The progression of the disease and the increasing severity of valvular regurgitation cause a volume overload of the left heart, leading to left atrial and ventricular remodeling and congestive heart failure (CHF). The treatment of chronic CHF secondary to MMVD in dogs has not always been the same over time. In the last fifty years, the drugs utilized have considerably changed, as well as the therapeutic protocols. Some drugs have also changed their intended use. An analysis of the literature concerning the therapy of chronic heart failure in dogs affected by this widespread degenerative disease is not available; a synthesis of the published literature on this topic and a description of its current state of art are needed. To the authors’ knowledge, a review of this topic has never been published in veterinary medicine; therefore, the aim of this study is to overview the treatments of chronic CHF secondary to MMVD in dogs from 1970 to 2020 using the general framework of narrative reviews.The treatment of chronic congestive heart failure (CHF), secondary to myxomatous mitral valve disease (MMVD) in dogs, has considerably changed in the last fifty years. An analysis of the literature concerning the therapy of chronic CHF in dogs affected by MMVD is not available, and it is needed. Narrative reviews (NRs) are aimed at identifying and summarizing what has been previously published, avoiding duplications, and seeking new study areas that have not yet been addressed. The most accessible open-access databases, PubMed, Embase, and Google Scholar, were chosen, and the searching time frame was set in five decades, from 1970 to 2020. The 384 selected studies were classified into categories depending on the aim of the study, the population target, the pathogenesis of MMVD (natural/induced), and the resulting CHF. Over the years, the types of studies have increased considerably in veterinary medicine. In particular, there have been 43 (24.29%) clinical trials, 41 (23.16%) randomized controlled trials, 10 (5.65%) cross-over trials, 40 (22.60%) reviews, 5 (2.82%) comparative studies, 17 (9.60%) case-control studies, 2 (1.13%) cohort studies, 2 (1.13%) experimental studies, 2 (1.13%) questionnaires, 6 (3.40%) case-reports, 7 (3.95%) retrospective studies, and 2 (1.13%) guidelines. The experimental studies on dogs with an induced form of the disease were less numerous (49–27.68%) than the studies on dogs affected by spontaneous MMVD (128–72.32%). The therapy of chronic CHF in dogs has considerably changed in the last fifty years: in the last century, some of the currently prescribed drugs did not exist yet, while others had different indications.

Efficacy and safety of berberine for congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy

This study was designed to assess the efficacy and safety of berberine for chronic congestive heart failure (CHF). One hundred fifty-six patients with CHF and >90 ventricular premature complexes (VPCs) and/or nonsustained ventricular tachycardia (VT) on 24-hour Holter monitoring were randomly divided into 2 groups. All patients were given conventional therapy for CHF, consisting of angiotensin-converting enzyme inhibitors, digoxin, diuretics, and nitrates. Patients in the treatment group (n = 79) were also given berberine 1.2 to 2.0 g/day. The remaining 77 patients were given placebo. Symptoms, a 6-minute walk test, left ventricular (LV) ejection fraction (EF), frequency and complexity of VPCs, and quality of life were assessed after 8 weeks of treatment and during a mean 24-month follow-up. After treatment with berberine, there was a significantly greater increase in LVEF, exercise capacity, improvement of the dyspnea–fatigue index, and a decrease of frequency and complexity of VPCs compared with the control group. There was a significant decrease in mortality in the berberine-treated patients during long-term follow-up (7 patients receiving treatment died vs 13 on placebo, p <0.02). Proarrhythmia was not observed, and there were no apparent side effects. Thus, berberine improved quality of life and decreased VPCs and mortality in patients with CHF.

Introduction

Introduction

Inotropic therapy for the failing myocardium.

Congestive heart failure (CHF) is a common clinical entity with diverse causes. Patients may present with acute decompensation or have a more indolent course, with diminishing exercise tolerance and increasing dyspnea. The management of this clinical entity traditionally has focused on restricting fluid intake, decreasing dietary sodium, decreasing afterload with vasodilatory agents, and supporting the failing myocardium with agents which produce a positive inotropic response. In the acutely decompensated patient, short-term therapy with positive inotropics is clearly beneficial. The role of long-term inotropic therapy for chronic CHF remains less clear. A number of clinical trials have recently evaluated the effects of long-term therapy on morbidity and mortality, with disappointing results. For a number of the newer, nonglycocide oral positive inotropics, at doses of drug which produce measurable hemodynamic improvement, increased mortality in treatment groups has been unacceptably high. Ironically, patients with worse left ventricular dysfunction show the most clinical improvement, but have the highest increased mortality. However, as with digoxin, there is some evidence that employing lower doses of drug that do not produce measurable improvement in hemodynamic parameters may result in both improved clinical state and decreased mortality. This review discusses the role of both oral and intravenous inotropic agents, discusses the difficulty in translating short-term hemodynamic improvement into long-term clinical benefit, and presents a rationale for the use of lower-dose inotropic therapy to improve long-term clinical outcome.

Platelet alpha 2 adrenoreceptors in chronic congestive heart failure

Patients with chronic congestive heart failure (CHF) are known to have elevated plasma concentrations of norepinephrine. Although this elevation of catecholamines in plasma may facilitate myocardial contractility, it may also be toxic to the myocardium in the long term. The alpha 2 adrenoreceptor located on noradrenergic nerve terminals regulates neuronal norepinephrine release by feedback inhibition. This receptor is also located on human blood platelets. This study determines the status of platelet alpha 2 adrenoreceptors in 16 patients with CHF (class I and II in 7 and class III and IV in 9) and in 26 normal volunteers. Specific high-affinity binding of the alpha 2 agonist 3H-clonidine and the alpha 2 antagonist 3H-yohimbine was used to determine the number (B max) of alpha 2 receptors and the dissociation constant (K D) for the 2 ligands. In the control population, the B max (in fmol/mg protein) for 3Hclonidine was 33 ± 2 and for 3H-yohimbine was 165 +- 12. There was a 25% difference in the maximum number of specific binding sites for 3H-clonidine in the class III/IV group (B max 24 ± 2, p < 3.05) and a 43% difference in the maximum number of specific binding sites for 3H-yohimbine (B max 94 ± 9; p < 0.005). There was a smaller but nonsignificant difference in the number of receptors on platelets from patients in the class I and II group. The K D's were similar in all 3 groups. These differences correlated well with the increases in plasma norepinephrine levels between the normal group (273.8 ± 44.1 pg/ml) and the class III/IV group (1333.5 ± 244.9, p < 0.0005). This study supports the hypothesis that increased levels of circulating norepinephrine in CHF lead to a decrease in platelet alpha 2 adrenoreceptors. Further studies should be performed to determine whether pharmacologic stimulation of these receptors might lead to a decrease in the neuronal release of that norepinephrine which might be toxic to the myocardium. Monitoring of platelet alpha 2 adrenoreceptor number may provide a guide to therapy of CHF.

Captopril in congestive heart failure: Improved left ventricular function with decreased metabolic cost

The oral angiotensin-converting enzyme inhibitor captopril (CPT) produces beneficial hemodynamic and clinical responses in patients with chronic congestive heart failure (CHF). Cardiac output and stroke volume increase, along with a decrease in pulmonary capillary wedge pressure, indicating improved left ventricular function. During maintenance CPT therapy, the beneficial hemodynamic and clinical effects appear to be sustained. Improved left ventricular pump function with CPT is associated with decreased metabolic cost, as myocardial oxygen consumption consistently decreases in proportion to the decrease in myocardial oxygen demand. Myocardial ischemia occurs infrequently, as is evident from the abnormal myocardial lactate metabolism. Hypotension appears to be the major adverse effect, particularly after the first dose. However, with dose titration and the use of a smaller initial dose, a marked precipitous fall in blood pressure can be avoided in the majority of patients. Thus, CPT may prove to be a useful agent in the vasodilator therapy of chronic CHF.

Postural hypotension during tilt with chronic captopril and diuretic therapy of severe congestive heart failure

The hemodynamic mechanism by which patients with chronic congestive heart failure (CHF) maintain their blood pressure (BP) in the upright posture is distinct from that of normal and hypertensive individuals. There are little data regarding the effects of chronic vasodilator therapy on the mechanisms controlling this response, especially in the presence of diuretic therapy. Therefore, 10 consecutive patients with severe chronic CHF underwent hemodynamic tilt study following acute and chronic captopril therapy. One patient developed orthostatic hypotension following first-dose captopril, but 6 of 10 had a mean BP decrease of 70 ± 6 to 56 ± 3 mm Hg on tilt following chronic captopril. This was associated with significant reduction of plasma aldosterone, and was abolished on re-tilt following acute saline infusion. Therefore, during chronic captopril therapy of CHF, a reduction of diuretic dosage may be necessary to prevent orthostatic hypotension.