Clinical Manifestations Of Heart Failure Research Articles

Prevention and management of chronic heart failure in management of asymptomatic patients

Symptomatic heart failure is preceded by a somewhat prolonged asymptomatic stage in many patients. The number of patients with asymptomatic heart dysfunction is about 4-fold greater than the number of patients with clinically overt heart failure. Pharmacologic treatment with angiotensin-converting enzyme inhibitors and β-blockers (in particular carvedilol) of asymptomatic patients with systolic left ventricular (LV) dysfunction can prevent or delay the occurrence of symptoms and reduce mortality in the long term. Thus, it would be of utmost importance to recognize and appropriately treat these patients before they develop heart failure symptoms. The cost-effectiveness of screening for asymptomatic heart dysfunction in the general population and in cohorts at risk has not been extensively evaluated. A normal electrocardiogram has a high negative predictive value in patients at risk. Echocardiography is the best tool for diagnosis and characterization of heart dysfunction, but extensive use is limited by availability and cost. Natriuretic peptides (brain natriuretic peptide and N-terminal pro–brain natriuretic peptide) are very sensitive markers of heart dysfunction and volume overload, and their measurement has been proposed as a first-line test to select patients who need echocardiography. The definition of the etiology of LV dysfunction—in particular, of the ischemic etiology—has prognostic and therapeutic implications. In addition to revascularization, pharmacologic treatment with antiplatelets and statins is helpful in preventing new ischemic events and the development of heart failure. The prevention, or at least the delay, of clinical manifestations of heart failure is strongly related to an effective approach to the asymptomatic stage. Therefore, it is important to educate the entire medical community, particularly physicians in the primary care setting, about recognition and treatment of these patients.

Evaluation of cardiac status in iron-loaded thalassaemia patients following bone marrow transplantation: improvement in cardiac function during reduction in body iron burden.

Iron-induced cardiac disease is the primary cause of death in transfused patients with thalassaemia major. The beneficial effects of deferoxamine mesylate on clinical cardiac disease have been well described but the impact of therapy on subclinical cardiac dysfunction is unknown. To assess the reversibility of subclinical cardiac dysfunction we studied the cardiac status during iron depletion treatment (phlebotomy) in iron overloaded patients, cured of thalassaemia by marrow transplantation, without clinical manifestation of heart failure but with alteration in both left ventricular diastolic function and in contractility property. 32 patients were studied and demonstrated a slight but significant impairment in the morphology and function if compared with matched normal controls. 17 of these patients were submitted to sequential echocardiographic evaluations during the phlebotomy programme. Following completion of the programme, normalization of the indices of contractility and normalization of diastolic function were observed. This study indicates that transplanted thalassaemia patients with subclinical left ventricular diastolic dysfunction and impaired left ventricular contractility may reverse these processes with an effective regimen of iron reduction such as phlebotomy.

The clinical diagnosis of heart failure in older patients.

To review the differences in presentation and clinical manifestation of heart failure in older and younger patients and to determine if these differences influence the ability to diagnose the disorder clinically. Based on this information, an approach to diagnosing heart failure in older patients is provided. Scientific reports regarding heart failure in both the general population and the geriatric population were identified from repeated searches of MEDLINE data base and citations from appropriate articles. Relevant data were obtained from articles, with special importance placed on studies designed to examine older patients exclusively or as a subgroup in a larger study. Review of data pertaining to clinical characteristics and presentation of heart failure was performed, with emphasis on comparing the characteristics between age groups. Specific cardiac diseases that cause ventricular impairment in older patients were assessed, and the importance of systolic versus diastolic dysfunction in this age group was analyzed. Clinical diagnosis of heart failure in older patients may be difficult because of the absence of typical symptoms and physical findings. When present, the symptoms and signs may be mistakenly diagnosed as caused by concomitant disorders or aging changes. In other older patients, the symptoms and signs will be obscured by the presence of aging changes or the presence of other diseases. As a result of these difficulties, the initial diagnosis of heart failure in older patients is made later in the course of the cardiac disease process; older patients will be more unstable, and secondary preventive therapies may be of less benefit than in younger patients with the disorder. Though clinically difficult, the differentiation between systolic and diastolic ventricular dysfunction is mandatory in all older patients with heart failure.

HEART FAILURE-INDUCED ADAPTATIONS IN CARDIAC AND SKELETAL MUSCLE: INSIGHTS FROM TRANSGENIC TO HUMAN MODELS 1369

Heart failure is a prevalent clinical problem that is very costly in both economic and humanitarian terms. Heart failure is a complex clinical syndrome in which deficits in both peripheral vascular and central cardiac function and regulation are observed. While the clinical manifestations of heart failure are multisystemic in nature, it is increasingly clear that myocardial failure is the proximal event in this clinical syndrome. Recent advances in the development of a variety of transgenic models of heart failure should prove useful in identifying the molecular etiology of myocardial failure and other mal-adaptations characteristic of the clinical syndrome of heart failure. Several murine models of heart failure bear remarkable phenotypic similarities to those observed in human heart failure. Expression of a mutant cardiac myosin heavy chain produces a hypertrophic cardiomyopathy model (HCM) in which compensatory cardiac hypertrophy progresses to severe ventricular dilation, wall thinning, and systolic dysfunction. Overexpression of a non-sarcomeric protein, myotonic dystrophy kinase, also produces an HCM phenotype. How transgenic animal models can be utilized in heart failure research will be an important theme of this symposium. Finally, since exercise intolerance is a hallmark symptom of heart failure that cannot be explained solely by an inability of the heart to deliver blood to the periphery, other contributing factors including abnormalities in the control of skeletal muscle blood flow and metabolism will be considered.

Afectación cardíaca en el sida

A great variety of cardiac disorders have been reported in HIV-infected patients: pericarditis, myocarditis, cardiomyopathies, endocarditis, cardiac involvement through malignancies, pulmonary hypertension, arrhythmias and thromboembolic disease. In general, these disorders are asymptomatic and often diagnosed in echocardiographic studies or autopsies. Pericardial involvement is the most common disorder. Pericardial effusions are asymptomatic and non-specific in a great proportion, but in some instances opportunistic infections or malignancies may lead to cardiac tamponade and are associated with an increased risk of mortality. The etiopathogenesis of myocarditis and cardiomyopathies is uncertain. There is controversy about the role of HIV as the primary etiologic agent. Opportunistic infections, cardiotoxic substances, nutritional deficiencies and autoimmune reactions have also been implicated as etiologic agents of myocardial damage. Short-term prognosis worsens as clinical manifestations of heart failure appear. Valvular involvement usually presents as marantic or infectious endocarditis, the latter most frequently in IVDU. This article reviews the main cardiovascular manifestations in AIDS.

Reduced Left Ventricular Contractile Reserve Identified by Low Dose Dobutamine Echocardiography as an Early Marker of Cardiac Involvement in Asymptomatic Patients with Thalassemia Major.

Patients with beta thalassemia major present with severe anemia and need continuous transfusion therapy. The consequent iron overload leads to hemochromatosis. Initial cardiac involvement can be present in thalassemic patients without clinical manifestations of heart failure. The purpose of this study was to assess the contractile reserve of the left ventricle in patients with normal baseline two-dimensional (2-D) echocardiographic findings using low dose dobutamine echocardiography. The underlying hypothesis was that, at an early stage, structural impairment of the myocardial wall due to myocardial iron deposits and/or secondary fibrotic changes could be so subtle so as not to impair resting systolic function, but is severe enough to blunt or even exhaust the contractile response to inotropic stimulation. Twenty-four consecutive patients (13 men and 11 women; ages 18 +/- 3.8 years) with beta thalassemia major undergoing evaluation for bone marrow transplantation entered the study. By selection, all were asymptomatic, without clinical signs of cardiac failure, and had normal regional and global systolic function at baseline echocardiographic study. A control group of 16 age and sex matched subjects was also studied. All underwent baseline, 2-D, and Doppler study, as well as dobutamine stress (up to 5 &mgr;g/kg per min) 2-D echocardiographic study. Patients and controls showed comparable values of indexes of global (ejection fraction: 0.64 +/- 0.06 vs 0.65 +/- 0.05, P = NS) and regional (systolic thickening of posterior wall: 90 +/- 34 vs 91 +/- 34%, P = NS) function at baseline. Left ventricular diastolic filling was evaluated with Doppler echocardiography. Peak flow velocity in early diastole was increased in thalassemic patients compared to controls (114 +/- 16 vs 96 +/- 18 cm/sec, P < 0.01), and flow velocity deceleration time was reduced (139 +/- 17 vs 157 +/- 20 msec, P < 0.01). At peak dobutamine, thalassemic patients showed a blunted contractile response compared to controls for indexes of both global (ejection fraction: 0.62 +/- 0.06 vs 0.69 +/- 0.05, P < 0.01) and regional (% systolic thickening of posterior wall: 91 +/- 36 vs 130 +/- 39%, P < 0.01) function. When individual patient analysis was performed, echocardiographic parameters were beyond the 95% confidence limits obtained from normal controls in 5 (21%) of the 24 study patients by one or more Doppler diastolic indexes, in 6 (25%) by indexes of contractile reserve, and in 11 (46%) by one of either diastolic function or contractile reserve indexes. These data demonstrate that the "iron heart" of asymptomatic thalassemic patients is a weak heart. Even if the regional and global systolic functions are similar to normals under resting conditions, the application of an inotropic challenge unmasks the weakness of these hearts, which can be identified at an earlier stage of their natural history through the blunted contractile response following the infusion of low dose dobutamine. The information on contractile reserve is not redundant, but rather incremental and in addition to that provided by Doppler echocardiographic indexes, which may be abnormal in these patients. (ECHOCARDIOGRAPHY, Volume 13, September 1996)

In search of ideal inotropic steroids: recent progress.

The need for new inotropic drugs follows from the prevalence of congestive heart failure in the developed countries, and from the fact that the cardiac drugs currently available are clearly inadequate to restore health or even to minimize discomfort and disability (review in [1]). In 1990, Kellermann [2] expected for the coming years that every effort must and will be made to further develop and create new compounds. These should not only beneficially affect the hemodynamic and functional impairment of patients with congestive heart failure, but also hopefully contribute to reaching an achievable goal, namely, the prevention of the clinical manifestations of heart failure. The arduous research, on the part of the pharmaceutical industry, to find a nonsteroidal “digitalis replacement” cannot be regarded as having been accomplished [3].The present review deliberately excludes the great number of cardioactive compounds of nonsteroidal types and divergent points of attack because they do not appear to promise progress in the treatment of cardiac failure (review in [4,5]). Taking the above demand as our challenge, we review in this chapter where we presently are in the search for ideal inotropic steroids. Earlier stages of this endeavor, documented elsewhere [6–8], will but cursorily be cited here. Our more recent approach has been derived from the hypothesis that the earlier failures in the synthetic further development of inotropic steroids with improved therapeutic range were based on the use of C/D-cis connected steroids as lead compounds which form the core in the medicinally used cardiac glycosides.

Angiotensin converting enzyme inhibition in asymptomatic left ventricular systolic dysfunction and early heart failure.

Benefit achieved through use of angiotensin converting enzyme (ACE) inhibitors in patients with reduced left ventricular (LV) systolic function is not confined to those with clinical manifestations of heart failure. Although rates of adverse clinical events are lower in asymptomatic patients, within this population ACE inhibitors have been shown to prevent adverse ventricular remodelling, prevent the development of clinical heart failure, reduce rates of hospitalization for heart failure and, in some studies, reduce mortality. Most of the benefit derived appears to be associated with preventing the progression of LV hypertrophy, dilatation, and dysfunction, resulting in prevention of heart failure. Additionally, the incidence of myocardial infarction is decreased, although the exact physiological basis for this benefit remains uncertain. Given the enormity and growth of heart failure as a public health problem and the potential for influencing the underlying pathophysiology, ACE inhibitor treatment offers substantial benefit for patients with asymptomatic LV systolic dysfunction.

Quantitative ultrasonic analysis of myocardium in patients with thalassemia major and iron overload.

Patients with beta-thalassemia major present with severe anemia and need continuous transfusion therapy. The consequent iron overload leads to hemochromatosis. Initial cardiac dysfunction has been documented even in thalassemics without clinical manifestations of heart failure as well as by conventional echocardiographic-Doppler techniques. The purpose of this study was to assess the acoustic quantitative properties of myocardium in patients with iron overload. Thirty-eight patients with beta-thalassemia major, without clinical signs of cardiac failure, and 20 age- and sex-matched young controls were studied by echocardiography. An on-line analysis of the ultrasonic radiofrequency signal was performed to obtain quantitative operator-independent measurements of the integrated backscatter (IB) signal of the ventricular septum and the posterior wall. The integrated values of the radiofrequency signal were normalized for the pericardial interface and expressed in percent (IB%). Thalassemic patients had been receiving transfusion therapy for 16 +/- 5 years and had received 313 +/- 138 transfusion units; they all had received chelation treatment (desferroxiamine) for 9 +/- 2 years. Patients and controls showed comparable values of echocardiographically assessed percent fractional shortening (32 +/- 3% versus 36 +/- 4%, p = NS), whereas thalassemics showed higher values of left ventricular mass index (118 +/- 30 versus 98 +/- 15 g/m2, p < 0.05). The IB% values were higher in patients with thalassemia major than in controls for both septum (35 +/- 14% versus 21 +/- 6%, p < 0.001) and posterior wall (16 +/- 6% versus 11 +/- 3%, p < 0.001). In thalassemic patients, no significant correlation was found between the septum IB% value and hematological parameters, such as the total number of transfusions (r = 0.2, p = NS) or the mean ferritin value (r = 0.1, p = NS). No significant correlation was also found between the septum IB% value and the echocardiographically assessed left ventricular mass index (r = 0.2, p = NS). These data demonstrate that myocardial reflectivity is abnormally increased in patients with thalassemia major under transfusion treatment, probably due to myocardial iron deposits and/or secondary structural changes. These quantitatively assessed abnormalities in regional reflectivity can be detected when conventional echocardiographic parameters of systolic left ventricular function are undistinguishable from normal controls.

Selective Beta-1-Adrenoceptor Partial Agonist Treatment for Congestive Heart Failure

Xamoterol is a beta-adrenoceptor partial agonist which selectively acts at the beta 1-receptors of the heart. The partial agonist effect modestly increases myocardial contractility and appears also to improve diastolic function and cardiac output without an increase in myocardial oxygen demand. Improved myocardial performance is maintained during exercise while increased heart rate is attenuated. Partial agonist activity protects against tachyphylaxis and arrhythmogenicity. With chronic treatment, exercise duration and work capacity increase and clinical manifestations of heart failure are reduced.

Late ventricular dilatation in survivors of acute myocardial infarction

The purpose of this study was to assess the natural course of left ventricular (LV) volumes in the convalescent phase of acute myocardial infarction (AMI). Fifty-seven patients were examined 2 weeks and approximately 1 year after AMI by a radionuclide method allowing determination of absolute LV volumes. After 1 year the patients had fewer clinical and radiologic signs of heart failure, but median end-diastolic volume index had increased from 92 to 112 ml/m 2 (p < 0.001), median end-systolic volume index from 51 to 65 ml/m 2 (p < 0.001) and median stroke volume index from 39 to 47 ml/m 2 (p < 0.001). Patients with first anterior infarcts had significantly greater increases in end-diastolic volume index, end-systolic volume index and stroke volume index than patients with first inferoposterior infarcts. The increase in LV volumes was significantly greater in patients with clinical manifestations of heart failure than in those without these signs. Notably, changes in LV size had an unpredictable effect on LV ejection fraction.

Treatment of pump failure in acute myocardial infarction

SOME degree of cardiac insufficiency occurs in most patients with acute myocardial infarction (MI), but in many, there are no important clinical consequences and therapy may be more harmful than useful. It is the patients whose clinical condition dictates the need for some therapeutic hemodynamic intervention with which this article will deal. <h3>Hemodynamic Monitoring</h3> Because MI usually involves the left ventricle, the early clinical manifestations of heart failure are usually those associated with either impaired oxygenation of the arterial blood owing to pulmonary congestion or inadequate peripheral perfusion owing to reduced cardiac output. Cardiogenic shock is an extreme example of both. Although cardiac failure can be recognized at the bedside, misinterpretation of clinical signs is not uncommon, particularly in patients with preexisting lung disease. Likewise, although it is usually possible to recognize inadequate peripheral perfusion at the bedside, the clinical findings associated with reduced cardiac output are not reliable in

Treatment of Pump Failure in Acute Myocardial Infarction

SOME degree of cardiac insufficiency occurs in most patients with acute myocardial infarction (MI), but in many, there are no important clinical consequences and therapy may be more harmful than useful. It is the patients whose clinical condition dictates the need for some therapeutic hemodynamic intervention with which this article will deal. <h3>Hemodynamic Monitoring</h3> Because MI usually involves the left ventricle, the early clinical manifestations of heart failure are usually those associated with either impaired oxygenation of the arterial blood owing to pulmonary congestion or inadequate peripheral perfusion owing to reduced cardiac output. Cardiogenic shock is an extreme example of both. Although cardiac failure can be recognized at the bedside, misinterpretation of clinical signs is not uncommon, particularly in patients with preexisting lung disease. Likewise, although it is usually possible to recognize inadequate peripheral perfusion at the bedside, the clinical findings associated with reduced cardiac output are not reliable in

Studies on Heart Failure in Old Age (Part 1) : Clinical and Hemodynamic Characteristics in Elderly Patients with Heart Failure

Hemodynamic characteristics were examined in elderly patients with heart failure. The results obtained are as follows: 1. Most of the underlying causes of heart failure in elderly patients were heart diseases which were commonly found in middle or od age. The onset of clinical manifestations of heart failure were in old age in most cases. 2. It was supposed that main factors which cause clinical manifestations were low cardiac output and low arterial oxygen tension rather than congestion in mild heart failure in old age. 3. In moderate or severe heart failure, cardiac output and arterial oxygen tension were markedly reduced, while venous pressure and total circulating blood volume were moderately increased. 4. Blood pressure was maintained due to elevation in total peripheral resistance in all stages of heart failure. 5. Aging changes contributed markedly to the hemodynamic changes in elderly patients with heart failure.

Improving the results of ligation of patent ductus arteriosus in small preterm infants

Thirty-two consecutive preterm infants with birth weights under 1,500 grams and with respiratory distress syndrome (RDS) complicated by a patent ductus arteriosus (PDA) underwent ligation of PDA. The indications for operation were massive left-to-right shunting associated with heart failure (cardiomegaly and pulmonary edema) unresponsive to medical treatment. The clinical manifestations of heart failure were related to the severity of RDS. Infants with mild-to-moderate RDS (21) often recovered and later developed typical findings of PDA (bounding pulses, hyperactive precordium, and murmur). They are now operated upon as soon as respiratory support is required. Infants with severe RDS (11) develop cardiomegaly earlier, and retrograde aortography may show massive left-to-right shunting before the presence of a murmur. Ligation is indicated when blood-gas values deteriorate despite medical treatment. Nineteen (59 per cent) of these extremely preterm infants survived to be discharged and 16 (50 per cent) are developing normally. Three have neurologic impariment. None of the survivors has clinical respiratory disease, and their radiologic findings of bronchopulmonary dysplasia are improving.

Left ventricular function in acute and chronic coronary artery disease.

The evaluation of left ventricular function in patients with acute myocardial infarction has shown: 1. Limitations in the use and interpretation of central venous pressure. 2. Pulmonary artery end-diastolic pressure reflects left ventricular end-diastolic pressure in the absence of pulmonary vascular or mitral valve disease. 3. Frequent elevations of left ventricular filling pressure in mild or clinically uncomplicated infarction. 4. Anterior infarctions present greater depression of left ventricular function than inferior infarctions. 5. Initial hemodynamic measurements in cardiogenic shock can predict prognosis with medical management. 6. Left ventricular function frequently improves during the early convalescent period. 7. Hemodynamic monitoring can be useful in following changes in left ventricular function and the response to therapy. The assessment of left ventricular performance in patients with chronic heart disease has shown: 1. Resting hemodynamic measurements are often normal but abnormalities can be observed in patients with disease of the left anterior descending coronary artery, diffuse coronary involvement, and after myocardial infarction. 2. Increases in end-diastolic volume or dilatation and left ventricular mass or hypertrophy can develop in severe coronary disease and after myocardial infarction. 3. The size of abnormally contracting segment after myocardial infarction is related to abnormalities in compliance, ventricular end-diastolic pressure, end-diastolic volume, and clinical manifestations of heart failure. 4. Exercise and atrial pacing can produce clinical and hemodynamic abnormalities. 5. The ejection fraction is significantly related to the slope of the ventricular function curve. 6. Angiographic abnormalities of left ventricular wall motion can be increased with atrial pacing and reduced with nitroglycerin or epinephrine.

Alterations of hemodynamics and myocardial mechanics in patients with congestive heart failure: Pathophysiologic mechanisms and assessment of cardiac function and ventricular contractility

HE FUNDAMENTAL PHYSIOLOGIC DERANGEMENTS, the disturbed events comprising cardiac contraction, the altered modulation of cardiovascular function, and the role of compensatory mechanisms in patients with congestive heart failure have been the subject of intense interest and investigation for many years. In the past, considerable attention has been focused on the clinical manifestations of heart failure and the hemodynamic alterations characteristic of this common pathologic condition. More recently, following the development of a multiplicity of improved technics and their application to experimental biologic systems and patients, a great body of new information has been provided which has permitted important advances in our understanding of the pathophysiology of congestive heart failure. Therefore, it is desirable at this time to examine certain of these findings, methods of evaluation, and current concepts concerning the mechanisms and regulation of contraction of the failing heart in man. This work begins with consideration of the principal determinants governing the performance of the intact ventricle and progresses to interpretation of the experimental data which form the basis for the conclusion that, of these major determinants, the fundamental abnormality in congestive heart failure

Thoracic duct-to-pulmonary vein shunt in the treatment of experimental right heart failure.

Elevated venous pressure in right heart failure leads not only to an increase in lymph formation but also to progressive resistance in the neck to the return of lymph to the circulation via the thoracic duct. Sequestration of fluid behind the failing heart tends to protect the circulation but at the same time leads to the clinical manifestations of heart failure. The present study was performed on 40 dogs with combined tricuspid insufficiency and pulmonary stenosis. Thoracic duct lymph flow was greatly increased. Pressure was considerably greater in the systemic veins than in the pulmonary vein beyond the right heart obstruction. Lymph flow was substantially enhanced when the thoracic duct was connected to the lower pressure pulmonary veins. Furthermore, direct anastomosis of the thoracic duct to the pulmonary vein resulted in fall in systemic venous pressure, increase in renal excretion of salt and water, and reduction in ascites. These results indicate that alterations in the flow of thoracic duct lymph have important bearing on the manifestations and treatment of right heart failure.

LEFT VENTRICULAR PERFORMANCE FOLLOWING DIGITALIZATION IN PATIENTS WITH AND WITHOUT HEART FAILURE.

Nine patients, three with left ventricular failure and six with compensated heart disease, were studied by means of right and transseptal left heart catheterization during acute digitalization with acetyl strophanthidin. One of the patients with heart failure and a compensated subject with the Wolff-Parkinson-White syndrome were also studied during supine left leg exercise. In the decompensated group, digitalization produced a decrease in heart rate and increases in stroke index, stroke work, mean stroke power, mean systolic ejection rate, and the rate of pressure rise in the left ventricle. Left ventricular end-diastolic pressures were markedly lowered after digitalization. In the compensated group, no significant changes in cardiac index, stroke index, or mean systolic ejection rate were observed. Although there were small increases in stroke work and power and moderate decreases in left ventricular diastolic pressures, the most striking finding was an increase in the rate of rise of left ventricular systolic pressure. Digitalization produced considerable improvement in the circulatory response to light exercise in a patient with left ventricular failure. Less marked improvement in the exercise response was observed in a patient with normal hemodynamics. After digitalization, left ventricular function points plotted on the stroke work end-diastolic pressure diagram tended to shift upward and to the left in both decompensated and compensated patients. The shift of function points was most prominent in the decompensated group. This study demonstrates that, in the presence of myocardial failure, acetyl strophanthidin markedly augments left ventricular performance. Furthermore, the data suggest that digitalization also improves left ventricular performance in patients with left ventricular enlargement but no clinical manifestations of heart failure.