Diastolic heart failure: Standard Doppler approach and beyond

Evidence of normal systolic left ventricular function has been reported in vp to 30-40% of patients with clinical signs of congestive heart failure, suggesting that diastolic dysfunction is an important predictor of prognosis and mortality. Doppler echocardiography as a noninvasive diagnostic procedure is able to provide immediate and relevant information on functional and structural changes underlying the clinical syndrome of heart failure. Four distinct early filling/late diastole (E/A) ratio patterns (normal, delayed relaxation, pseudonormal, restrictive) can be discerned if viewed within the context of other available clinical information. These patterns evolve from one to another in a single individual, with changes in disease evolution, treatment, and loading condition. They represent a continuum from normal to severe diastolic dysfunction, showing progressively increasing left ventricular (LV) chamber stiffness and subsequently decreasing deceleration time. The combination of Doppler restrictive filling pattern and decreased deceleration time provides important information that helps to differentiate gradations of diastolic dysfunction and has been found to be a potent predictor of prognosis and mortality in various cardiac conditions. When clinical and transthoracic data alone are not sufficient in guiding therapy of congestive heart failure, transesophageal echocardiography can be used to assess most Doppler flows, especially pulmonary venous and left atrial (LA) appendage flows. The use of the multiplane transducer in multiple intermediate scan planes further improves the possibility of optimizing the Doppler incident angle and obtaining the best Doppler recordings of the left upper or right upper pulmonary venous flow. Whereas LV diastolic dysfunction is common in patients with congestive heart failure and appears to be an important predictor of prognosis, little information is available about right ventricular (RV) diastolic dysfunction, The role of RV function in congestive heart failure has probably been underestimated and it is possible that RV diastolic dysfunction assessment is equally important in the follow-up of heart failure patients. Recently, 2 novel echocardiographic technologies for the assessment of ventricular wall dynamics have been developed-color kinesis and tissue Doppler imaging. Both techniques have recently been shown to provide global as well as regional information on LV contraction and filling. Complementary use of both techniques may allow a more complete noninvasive assessment of global and regional systo-diastolic LV function, (C) 1998 by Excerpta Medico, Inc

Vasopressin Antagonism in Heart Failure

Treatment of chronic heart failure (HF) is based on interference with the renin-angiotensin-aldosterone system and the adrenergic nervous system. Diuretics are used in volume-expanded patients. Insights from clinical trials and registries establish the need to consider correcting both cardiac loading conditions and nonload-related biological factors if HF therapy is to be optimized. Arginine vasopressin (AVP) represents a potentially attractive target for therapy in both acute and chronic HF. Excessive AVP secretion could contribute to both systolic and diastolic wall stress via V1a- and V2-mediated effects on the peripheral vasculature and on water retention. Arginine vasopressin also may directly and adversely affect myocardial function due to the effect of V1a activation on myocardial contractility and cell growth. Last, AVP may contribute to hyponatremia, a powerful predictor of poor outcome in HF. The development of effective nonpeptide antagonists to both the V1a and V2 receptors for AVP now allows for testing the hypotheses that interfering with AVP-mediated signaling could be beneficial in HF. This review summarizes the theoretical rationale for further development of such therapy, reviews the status of current compounds under development, and suggests key issues that need to be addressed as these agents undergo further clinical testing

Pathophysiology of Heart Failure

Heart failure occurs when the heart is unable to maintain a cardiac output sufficient to satisfy the oxygen requirements of the body despite adequate blood volume and hemoglobin content. Regardless of the initial cause of heart failure and in spite of compensatory mechanisms, patients often follow a course of worsening heart failure that is characterized by a low cardiac output, high filling pressures, and increased peripheral vascular resistance. In addition to persistence of the initiating event, cardiac deterioration may be caused or aggravated by a variety of factors including depletion of cardiac norepinephrine stores, down-regulation of myocardial beta-adrenergic receptors, microvascular spasm with resultant further cellular necrosis, and subendocardial ischemia perpetuating myocardial failure

Acute Dyspnea and Decompensated Heart Failure

The majority of patients hospitalized with acute heart failure (AHF) initially present to the emergency department (ED). Correct diagnosis followed by prompt treatment ensures optimal outcomes. Paradoxically, identification of high risk is not the unmet need, given nearly all ED AHF patients are hospitalized; rather, it is identification of low-risk. Currently, no risk-stratification instrument can be universally recommended to safely discharge ED patients. With the exception of diagnosis, management recommendations are largely expert opinion, informed by existing evidence and tradition. In the absence of robust evidence, we propose a framework for management to guide the busy clinician

Aldosterone Receptor Blockade in Patients with Left Ventricular Systolic Dysfunction Following Acute Myocardial Infarction

Left ventricular systolic dysfunction (LVSD) is a common complication of acute myocardial infarction (AMI) that occurs in approximately 30% of post-AMI patients, and results in a threefold increase in in-hospital and 6-month mortality, regardless of type of AMI. Post-AMI care has evolved to include early reperfusion, antiplatelet therapy, hydroxymethylglutaryl coenzyme A reductase inhibitors (stains), beta blockers, angiotentsin-converting enzyme inhibitors, and angiotensin receptor blockers. Despite these therapies, however, there is still an excess of sudden cardiac death (SCD), especially in patients with severe LVSD and in the first 30 days post-AMI. Aldosterone has been shown to be elevated in patients with post-AMI LVSD and to have deleterious effects on the myocardium, including endothelial dysfunction, collagen deposition, inflammation, apoptosis, and autonomic instability, leading to left ventricular remodeling and SCD. Aldosterone blockade with eplerenone has been shown to reduce mortality even in the presence of optimal post-AMI therapy in patients with post-AMI LVSD. Despite this, eplerenone is underutilized in real-world clinical practice. Care must be taken to follow renal function and potassium balance in patients treated with eplerenone. © 2008 Elsevier Inc. All rights reserved