Heart failure monitor最新文献

Left ventricular (LV) remodeling, which can result from myocardial damage or ventricular pressure or volume overload, has genomic, cellular, and interstitial components with associated changes in ventricular size, shape, wall thickness, and function. It is a process that is detectable and measurable clinically, generally progressive, and associated with adverse outcomes. However, it is amenable to intervention, prevention, or reversal. Following myocardial infarction (MI), LV remodeling is particularly likely in patients with transmural or anterior infarction and in those with failed reperfusion or LV failure. Infarct artery patency and neurohormonal blockade are key management considerations for prevention or reversal of LV remodeling. Combination treatment with angiotensin-converting enzyme inhibition and beta-blockade is of proven benefit following MI, improving LV remodeling and long-term outcomes.

Heart failure is one of the leading causes of hospitalization worldwide. Mitral regurgitation (MR) is a known complication of end-stage cardiomyopathy and is associated with a poor prognosis. Historically, these patients were managed medically and frequently with mitral valve replacement, both of which have unfavorable long-term outcomes. Over a 10-year period, we studied 167 patients with cardiomyopathy and severe MR who underwent mitral valve repair. These patients with 4+ MR, a mean left ventricular ejection fraction (LVEF) of 14+/-6 and New York Heart Association (NYHA) class III or IV congestive heart failure (CHF) were prospectively studied. All patients underwent mitral valve repair with an undersized annuloplasty ring. There was one intra-operative death and eight 30-day mortalities. Intra-operative echocardiography revealed no MR in most patients and trivial to mild MR in seven patients. There were 26 late deaths; two of these patients had progression of CHF and underwent transplantation. The 1-, 2-, and 5-year actuarial survival rates were 82%, 71%, and 52%, respectively. NYHA class was improved for all patients from a pre-operative mean of 3.2+/-0.2 to 1.8+/-0.4 postoperatively. At 24-month follow-up, all patients demonstrated improvement in LVEF, cardiac output, and end-diastolic volume, with a reduction in sphericity index and regurgitant volume. Mitral valve repair utilizing an undersized annuloplasty ring is safe and effectively corrects MR in cardiomyopathic patients. All of the observed changes contribute to reverse remodeling and restoration of the normal LV geometric relationship. Mitral valve repair offers a new strategy for patients with MR and end-stage cardiomyopathy.

B-type natriuretic peptide (BNP) is a neurohormone synthesized in the cardiac ventricles. It is released as N-terminal pro-BNP (NT-proBNP) and cleaved enzymatically to the NT fragment and the immunoreactive BNP. Measurement of BNP is now available as a rapid bedside assay that is easily available to physicians in an office, clinic, emergency department, or inpatient setting. It has proven utility in the emergency department diagnosis of congestive heart failure (CHF) in patients with unclear causes of dyspnea. The use of BNP level as a criterion for hospital admission has been studied as has its use as an aid in decision-making regarding the adequacy of treatment and readiness for hospital discharge. Treatment of chronic CHF in outpatients using BNP as a guide for the intensity of pharmacological therapy shows promise in further decreasing the rate of adverse events associated with this diagnosis. Other uses for BNP measurement include the prognostication of CHF exacerbation and myocardial infarction, and screening those at risk to identify patients that may benefit from early intervention and treatment of early CHF.

Over 4.7 million Americans have heart failure, and 50000 new cases of heart failure are diagnosed every year. In addition, a significant proportion of the population may have asymptomatic left ventricular (LV) systolic dysfunction. Population studies estimate that the prevalence of asymptomatic LV dysfunction ranges from 0.9-5.9%. Of these, a substantial number will eventually develop symptomatic heart failure. Diagnosing and treating these patients before they develop symptoms may help to delay or prevent the development of symptomatic heart failure. This review highlights the currently available data on the epidemiology, pathophysiology, diagnosis, and treatment of asymptomatic LV systolic dysfunction.

Iatrogenic infarction of the hypertrophic intraventricular septum in hypertrophic obstructive cardiomyopathy has become an accepted treatment for patients refractory to medical treatment and/or pacemaker therapy. During the 8 years of its existence, non-surgical myocardial reduction (NSMR), which is based on the injection of absolute alcohol into the first or second septal perforator originating from the left anterior descending coronary artery, has been used more frequently than surgical myectomy. The advantages of this catheter procedure are local anesthesia, short hospital stay, and less morbidity as compared with open heart surgery. Patients with an interventricular septal thickness of at least 18 mm, left ventricular outflow tract gradient at rest of at least 30 mmHg, and an intraventricular gradient during provocation (such as isoproterenol, dobutamine, amylnitrate, and postextrasystolic potentiation) are potential candidates for this procedure. Important mitral valve abnormalities must be excluded prior to septal ablation with alcohol. In some patients, the coronary anatomy is unsuitable for this procedure. Mid-to-long-term results have shown very significant intraventricular gradient reduction, symptom improvement, reduction in left ventricular filling pressure and pulmonary artery pressure, and increase in exercise capacity. Complications, such as the need for long-term pacing, have fallen with the reduction of the total amount of injected alcohol and the use of contrast echocardiography. NSMR appears to be effective, and can be used as an alternative to classical surgical myectomy in symptomatic patients resistant to conservative treatment.

Experimental and clinical studies have recently demonstrated that the growth hormone-insulin-like growth factor-I (GH-IGF-I) system is involved in the regulation of cardiac structure and function. Patients with acromegaly have an increased propensity of developing cardiovascular complications, such as ventricular hypertrophy with interstitial fibrosis. Conversely, patients with GH deficiency can exhibit ventricular dysfunction, increased vascular thickness, and an increased number of atheromatous plaques. In both groups of patients these abnormalities may be partially reverted by normalizing GH-IGF-I levels. In experimental or human chronic heart failure (CHF), GH administration increases ventricular mass and cardiac performance and reduces pulmonary vascular resistance. The mechanism by which this occurs is still unclear, but seems to involve calcium channels and non-endothelium-mediated vasodilatation. Randomized trials studying CHF patients contradict these results, highlighting that, in patients with heart failure, the response to GH therapy appears to be variable, and is probably influenced either by acquired GH resistance or by baseline levels of hormones. Due to the small number of patients examined to date, larger, randomized, controlled studies are needed.

Angiotensin II type I receptor antagonists (ARAs) have been tested in two large randomized trials, Evaluation of Losartan in the Elderly II (ELITE II) and the Valsartan Heart Failure Trial (Val-HeFT), and several other large trials are ongoing in the indication of chronic heart failure (CHF). Based on the available evidence, angiotensin converting enzyme inhibitors remain the cornerstone in the treatment of CHF. However, much more information should be available in the next few years, which will provide more evidence on how to use ARAs and in which patients.

There were almost 1 million hospitalizations for heart failure in 1999, representing a 155% increase over the last 20 years, and the treatment of these patients is an important and growing problem. However, currently available therapies, which are based on three basic mechanisms of action (diuresis, exogenous vasodilators, and cyclic adenosine monophosphate-dependent positive inotropes), have significant limitations that have encouraged the development of newer agents. The leading medications for this indication are representatives of three different therapeutic approaches, which include endogenous vasodilatory neurohormones (nesiritide), calcium sensitizers (levosimendan), and neurohormonal antagonists (tezosentan). These three agents represent a new generation of therapeutics for this important medical problem and may provide the means not only to treat symptoms, but also to improve longer-term clinical outcomes.

The incidence of chronic heart failure (CHF) has been increasing, particularly because of the aging of the population and the improved survival of patients with coronary artery disease. Therefore, the current pathophysiological and clinical considerations in the diagnosis and treatment of CHF will need further improvement in terms of cardiovascular risk profiling, preventive measures, earlier intervention, and patient-tailored disease management. To date, the role of the kidney in CHF is mainly considered within the context of excessive salt and water retention, due to reduced renal blood flow. However, recent data indicate that the kidney may play a more decisive role in the progression and prognosis of the disease. It has been demonstrated that renal function is independently associated with an increased risk for all-cause mortality and cardiovascular morbidity. Furthermore, moderate renal insufficiency is a common phenomenon in this patient population and, for example, left ventricular ejection fraction, glomerular filtration rate, and New York Health Association class are not only prognostically important but are also acting independently, and support the hypothesis that cardiac function, clinical status, and renal function represent, in part, different prognostic entities of CHF. It could be questioned why an impaired renal function adds prognostic risk to develop CHF? A subclinically decreased renal function is unlikely to be the direct cause. Renal function is known to correlate with a variety of cardiovascular risk factors. Similar risk factors could contribute to the pathogenesis of intrarenal disease. Furthermore, a large number of metabolic abnormalities are related to impaired renal function and induce myocardial dysfunction and damage. Finally, neurohormonal activation is apparent in patients with chronic heart failure. Angiotensin II, the central product of the renin-angiotensin system, may play a central role in the pathophysiology and progression of cardiovascular and renal diseases. In conclusion, to prevent cardiovascular morbidity and mortality, new therapeutic strategies might be triggered by focussing on increasing our knowledge concerning adaptive and maladaptive mechanisms of the kidney involved in CHF.