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Digitalis for treatment of congestive heart failure in patients in sinus rhythm.

BACKGROUND: Digitalis glycosides have been in clinical use in the treatment of congestive heart failure (CHF) for more than 200 years. In recent years several trials have been conducted to address concerns about efficacy and toxicity. Although a systematic review of the literature was published in 1990, an update is required to include more current trials. OBJECTIVES: To examine the effectiveness of digitalis glycosides in treating CHF in patients with normal sinus rhythm. To examine the effect of digitalis in patients taking diuretics, angiotensin converting enzyme inhibitors, and beta-blockers; patients with varying severity and duration of disease; patients with prior exposure to digitalis vs. no prior exposure; and patients with "CHF due to systolic dysfunction" vs. "CHF with preserved systolic function." SEARCH STRATEGY: The Cochrane Central Register of Controlled Trials (CENTRAL) 2003 Issue 4, MEDLINE (1966 to December 2003) and EMBASE (1990 to December 2003) were searched. Dissertation Abstracts and annual meeting abstracts of the American Heart Association, American College of Cardiology, and European Society of Cardiology were also searched from 1996-2003. In addition, reference lists provided by the pharmaceutical industry (Glaxo Wellcome Inc.) were searched. SELECTION CRITERIA: Included were randomized placebo-controlled trials of 20 or more adult patients of either sex with symptomatic CHF who were studied for seven weeks or more. Excluded were trials in which the prevalence of atrial fibrillation was 2% or greater, or in which any arrhythmia that might compromise cardiac function or any potentially reversible cause of CHF such as acute ischemic heart disease or myocarditis was present. DATA COLLECTION AND ANALYSIS: Articles selected from the searches described above were evaluated as a joint effort of the coauthors. The staff of the Cochrane Heart Group ran searches on the Cochrane Central Register of Controlled Trials. MAIN RESULTS: Thirteen articles meeting the defined criteria were identified, and major endpoints of mortality, hospitalization, and clinical status, based respectively upon 8, 4, and 12 of these selected studies, were recorded and analyzed. The data show that there is no evidence of a difference in mortality between treatment and control groups, whereas digitalis therapy is associated with a lower rate of hospitalization and of clinical deterioration. REVIEWERS' CONCLUSIONS: The literature indicates that digitalis has a useful role in the treatment of patients with CHF who are in normal sinus rhythm.

Cardiotonic Agents↗

Effect of exercise and cavity size on right ventricular function in morbid obesity.

To assess the effect of exercise and to determine the influence of the right ventricular (RV) internal dimension on RV systolic function in morbid obesity, M-mode and 2-dimensional echocardiography and radionuclide ventriculography were performed on 22 patients whose body weight was at least twice the ideal body weight and who had no clinical or laboratory evidence of underlying organic heart disease or pulmonary disease. RV ejection fraction was measured at rest and during peak supine bicycle exercise. RV exercise response was defined as the change in RV ejection fraction during peak exercise. There was a significant negative correlation between percent over ideal body weight and RV exercise response (r = 0.86, p less than 0.00005) and between RV internal dimension and RV exercise response (r = 0.60, p less than 0.005). There were significant positive correlations between resting RV and left ventricular (LV) ejection fraction (r = 0.56, p less than 0.01) and between RV and LV exercise response (r = 0.70, p less than 0.0005). The subgroup with a high-normal or enlarged RV internal dimension (greater than or equal to 2.0 cm, n = 10) experienced no significant change in RV ejection fraction with exercise, whereas the subgroup whose RV internal dimension was less than 2.0 (n = 12) experienced a significant increase in RV ejection fraction from 44 +/- 10% at rest to 58 +/- 11% at peak exercise (p less than 0.03). The results suggest that in morbidly obese individuals without underlying cardiopulmonary disease RV dilatation may predispose to RV systolic dysfunction and assessment of RV systolic function should optimally include evaluation of RV exercise response.

Adult↗

Brain natriuretic peptide predicts right heart failure in patients with acute pulmonary embolism.

BACKGROUND: Plasma levels of brain natriuretic peptide (BNP) are increased in patients with left heart failure. In patients with severe pulmonary embolism (PE), primary right ventricular (RV) dysfunction is frequent. Little is known about BNP secretion in acute RV failure. METHODS: We prospectively studied 50 consecutive patients with confirmed PE (age range, 57 +/- 19 years; 36 men). PE was confirmed with pulmonary angiography, spiral computed tomography, or echocardiography and subsidiary analyses. On admission, echocardiography and BNP measurements were performed in all patients. RESULTS: Patients without RV dysfunction had significantly lower BNP levels than patients with RV dysfunction (55 +/- 69 pg/mL vs 340 +/- 362 pg/mL, P <.001). There was a significant correlation between RV end-diastolic diameter and BNP (r = 0.43, P <.05). BNP discriminated patients with or without RV dysfunction (area under the receiver operating characteristic curve, 0.78; 95% CI, 0.64-0.92). A BNP >90 pg/mL was associated with a risk ratio of 28.4 (95% CI, 3.22-251.12) for the diagnosis of RV dysfunction. All patients without LV systolic dysfunction who had syncope necessitating cardiopulmonary resuscitation had normal BNP levels. Patients with RV dysfunction had significantly more in-hospital complications (cardiogenic shock, inotropic therapy, mechanical ventilation). However, BNP levels were not predictive of mortality or in-hospital complications. CONCLUSIONS: BNP levels are frequently increased in patients with PE who have RV dysfunction, whereas patients without RV dysfunction show reference range BNP levels in the absence of left ventricular dysfunction. In acute PE, BNP elevation is highly predictive of RV dysfunction, but not of in-hospital complications and mortality.

Acute Disease↗

Congestive heart failure in the elderly. The therapeutic challenge of atypical presentations.

Congestive heart failure (CHF) is a common cause of morbidity and mortality in the elderly. Symptoms and signs of CHF in the elderly often differ from those in younger patients. Careful attention to these subtle differences helps in detection of concomitant illnesses that mimic or mask heart failure. The therapeutic approach to CHF in elderly patients is similar to that in younger patients. However, in the elderly, increased attention should be paid to the side effects and interactions of the drugs commonly prescribed. Diastolic dysfunction is a recently recognized factor in the pathogenesis of CHF. Because diastolic dysfunction is treated differently than systolic dysfunction, evaluation of CHF should include a search for both entities.

Aged↗

The perindopril in elderly people with chronic heart failure (PEP-CHF) study.

AIMS: Many patients who receive a diagnosis of heart failure have neither a low left ventricular (LV) ejection fraction nor valve disease. Few substantial randomized controlled trials have been conducted in this population, none has focussed on patients with evidence of diastolic dysfunction and none has shown clear benefit on symptoms, morbidity, or mortality. METHODS AND RESULTS: This was a randomized double-blind trial, comparing placebo with perindopril, 4 mg/day in patients aged > or =70 years with a diagnosis of heart failure, treated with diuretics and an echocardiogram suggesting diastolic dysfunction and excluding substantial LV systolic dysfunction or valve disease. The primary endpoint was a composite of all-cause mortality and unplanned heart failure related hospitalization with a minimum follow-up of 1 year. A total of 850 patients were randomized. Their mean age was 76 (SD 5) years and 55% were women. Median follow-up was 2.1 (IQR 1.5-2.8) years. Enrollment and event rates were lower than anticipated, reducing the power of the study to show a difference in the primary endpoint to 35%. Many patients withdrew from perindopril (28%) and placebo (26%) after 1 year and started taking open-label ACE-inhibitors. Overall, 107 patients assigned to placebo and 100 assigned to perindopril reached the primary endpoint (HR 0.919: 95% CI 0.700-1.208; P = 0.545). By 1 year, reductions in the primary outcome (HR 0.692: 95% CI 0.474-1.010; P = 0.055) and hospitalization for heart failure (HR 0.628: 95% CI 0.408-0.966; P = 0.033) were observed and functional class (P < 0.030) and 6-min corridor walk distance (P = 0.011) had improved in those assigned to perindopril. CONCLUSION: Uncertainty remains about the effects of perindopril on long-term morbidity and mortality in this clinical setting since this study had insufficient power for its primary endpoint. However, improved symptoms and exercise capacity and fewer hospitalizations for heart failure in the first year were observed on perindopril, during which most patients were on assigned therapy, suggesting that it may be of benefit in this patient population.

Aged↗

Cell death in acromegalic cardiomyopathy.

BACKGROUND: Prolonged untreated acromegaly leads to a nonspecific myopathy characterized by ventricular dysfunction and failure. However, the mechanisms responsible for the alterations of cardiac pump function remain to be defined. Because cell death is implicated in most cardiac disease processes, the possibility has been raised that myocyte apoptosis may occur in the acromegalic heart, contributing to the deterioration of ventricular hemodynamics. METHODS AND RESULTS: Ten acromegalic patients with diastolic dysfunction and 4 also with systolic dysfunction were subjected to electrocardiography, Holter monitoring, 2-dimensional echocardiography, cardiac catheterization, and biventricular and coronary angiography before surgical removal of a growth hormone-secreting pituitary adenoma. Endomyocardial biopsies were obtained and analyzed quantitatively in terms of tissue scarring and myocyte and nonmyocyte apoptosis. Myocardial samples from papillary muscles of patients who underwent valve replacement for mitral stenosis were used for comparison. The presence of apoptosis in myocytes and interstitial cells was determined by confocal microscopy with the use of 2 histochemical methods, consisting of terminal deoxynucleotidyl transferase (TdT) assay and Taq probe in situ ligation. Acromegaly was characterized by a 495-fold and 305-fold increase in apoptosis of myocytes and nonmyocytes, respectively. The magnitude of myocyte apoptosis correlated with the extent of impairment in ejection fraction and the duration of the disease. A similar correlation was found with the magnitude of collagen accumulation, indicative of previous myocyte necrosis. Myocyte death was independent from the hormonal levels of growth hormone and insulin-like growth factor-1. Apoptosis of interstitial cells did not correlate with ejection fraction. CONCLUSIONS: Myocyte cell death, apoptotic and necrotic in nature, may be critical for the development of ventricular dysfunction and its progression to cardiac failure with acromegaly.

Acromegaly↗

The effects of cardioversion and defibrillation on left ventricular systolic function.

The purpose of this research was to evaluate the left ventricular systolic function behavior after cardioversion and defibrillation. The study included 18 adult patients who had direct current cardioversion or defibrillation performed for conversion of spontaneous or induced arrhythmias. All patients were submitted to a careful medical evaluation and an M-mode echocardiogram before cardioversion or defibrillation. The clinical and echocardiographic evaluations were repeated immediately after, and 6 and 12 h following the countershock. Six hours after cardioversion or defibrillation a statistically significant (p = .04) decrease in contractility (circumferential fiber shortening and ejection fraction) was observed without significant changes in preload (end diastolic volume), heart rate or afterload (end systolic stress and diastolic arterial pressure). Within 12 h, the left ventricular systolic dysfunction disappeared. The impairment of systolic function was independent of the amount of energy used, the type of arrhythmia, the rhythm after cardioversion or defibrillation and the etiologic cardiac diagnoses. There was a significant (p = .03) direct, negative and linear correlation between left ventricular systolic indices (ejection fraction and circumferential fiber shortening) before the countershock and the amount of decrease in systolic function after the countershock. In spite of the fact that most patients had a low ejection fraction, none of them presented clinical signs of heart failure. Defibrillation and cardioversion produce a transient decrease in cardiac contractility which is independent of the amount of energy used and does not produce clinical signs of heart failure.

Arrhythmias, Cardiac↗

Diabetic cardiomyopathy. A unique entity or a complication of coronary artery disease?

The increased incidence of congestive heart failure and the increased mortality and morbidity in the diabetic patient following myocardial infarction or coronary artery bypass graft can be explained by the presence of diabetic cardiomyopathy. Noninvasive studies in young diabetic patients show no cardiac abnormality, but in older diabetic patients mild cardiac diastolic dysfunction is detectable. This mild cardiomyopathy can become clinically detectable in the presence of hypertension and can be severe in the presence of myocardial ischemia. Microvascular disease is unlikely to cause diabetic cardiomyopathy. Cellular changes, including defects in calcium transport and fatty acid metabolism, may lead to myocellular hypertrophy and myocardial fibrosis, initially causing diastolic dysfunction that may advance to systolic dysfunction. Glycemic control, energetic detection and treatment of hypertension with appropriate antihypertensive agents, and early detection and treatment of ischemic heart disease are essential in preventing and treating diabetic cardiomyopathy.

Animals↗

[The use of tissue Doppler imaging for the diagnosis of restenosis after percutaneous coronary revascularisation].

UNLABELLED: OBJECTIVE AND AIM OF THE STUDY: Diagnosis of restenosis after percutaneous transluminal coronary angioplasty (PTCA) is difficult due to low sensitivity and specificity of widely used methods. The aim of the study was to evaluate the usefulness of tissue Doppler Imaging (TDI) in the diagnosis of restenosis in comparison with the results of clinical examination, electrocardiographic exercise test (ETT) and wall motion score index (WMSI) analysis. MATERIAL AND METHODS: 22 patients (18 males, 4 females) aged 46-69 with coronary artery disease who underwent PTCA, with restenosis of widen artery found during one-year follow-up. The angioplasty of anterior descending artery was made in 16 patients, circumflex artery was widened in 2 patients, right coronary artery in 4 patients. Clinical and echocardiographic examinations, ETT and TDI were made in all the patients before PTCA, one month after PTCA and during restenosis before control coronary angiography. In TDI examination maximal systolic and maximal early diastolic velocities of myocardium were determined in 18 left ventricle segments. RESULTS: After the procedure significant decrease of clinical symptoms and ST depression during ETT were found. Restenosis resulted in recurrence of clinical symptoms and ETT parameter worsening. No significant changes in the mean values of left ventricle ejection fraction was observed after PTCA or during restenosis. Mitral inflow E/A ratio was decreased before PTCA, after PTCA and during restenosis. In 12 (55%) patients despite significant coronary artery stenosis, WMSI was normal (1.0) both before PTCA, after PTCA and during restenosis. In 10 (45%) patients with anterior descending artery stenosis regional contractility disturbances were found before PTCA. After revascularisation WMSI decreased in only 4 patients. During TDI examination in patients with contractility disturbances before PTCA, revascularisation resulted in significant systolic myocardial velocity increase, and restenosis was manifested by renewed systolic myocardial velocity decrease. Early diastolic myocardial velocities in ischaemic segments were significantly decreased before PTCA in all the patients, and no increase were found despite effective PTCA. CONCLUSIONS: Significant coronary artery stenosis leads to left ventricle diastolic function disturbances, however may not result in systolic dysfunction. After PTCA procedure significant systolic left ventricle function improvement, expressed by increase of systolic myocardial velocity in ischaemic segments, no changes of diastolic left ventricle function is seen. Restenosis in patients after PTCA is manifested by renewed decrease of systolic myocardial velocity in ischaemic segments.

Aged↗

Cardiovascular diseases in obstructive sleep apnea.

Obstructive sleep apnea (OSA) affects approximately 5% of women and 15% of men in the middle-aged adults, and associated with adverse health outcomes. Cardiovascular disturbances are the most serious complications of OSA. These complications include heart failure, left/right ventricular dysfunction, acute myocardial infarction, arrhythmias, stroke, systemic and pulmonary hypertension. All these cardiovascular complications increase morbidity and mortality of OSA. Several epidemiologic studies have demonstrated that sleep related breathing disorders are an independent risk factor for hypertension, probably resulting from a combination of intermittent hypoxia and hypercapnia, arousals, increased sympathetic activity, and altered baroreflex control during sleep. Arterial hypertension, obesity, diabetes mellitus and coronary artery disease (CAD) which are independent predictors of left ventricular dysfunction, often have co-existence with OSA. Especially severe OSA patients having diastolic dysfunction might have an increased risk of heart failure, since diastolic dysfunction might be combined with systolic dysfunction. Early recognition and appropriate therapy of ventricular dysfunction is advisable to prevent further progression to heart failure and death. Patients with acute myocardial infarction, especially if they had apneas and hypoxemia without evident heart failure should be evaluated for sleep disorders. So, patients with CAD should be evaluated for OSA and vice versa. Early recognition and treatment of OSA may improve cardiovascular functions. Continuous positive airway pressure (CPAP) applied by nasal mask, is still the gold standard method for treatment of the disease and prevention of complications.

Cardiovascular Diseases↗

Ventricular and myocardial efficiencies during acute aortic regurgitation in conscious dogs.

BACKGROUND: Alterations in cardiac efficiency may signal pathologic stresses and energetic adaptation during aortic regurgitation (AR). METHODS AND RESULTS: LV systolic function, left coronary blood flow, and AVO2 difference were measured in conscious dogs to assess LV and contractile efficiencies at baseline, 1 day (n=10), 1 week (n=10), and 3 weeks (n=8) of AR. LV systolic function was assessed by the preload recruitable stroke work relationship. Total LV Efficiency (TEFF=SWxHeart Rate/MVO2) and contractile efficiency (CEFF=1/the slope of the MVO2 -pressure-volume area relationship) and steady-state potential energy (PVA-SWxHR), mechanical coupling efficiency (MCE=SWxHR/PVA) were calculated. LV systolic function decreased by 17% at 1 day (P<.05) and by 24% at 3 weeks (P<.05). CEFF decreased from 58+/-8% to 38+/-10% (P<.05) at 1 day, normalized at 1 week, and decreased to 28+/-14% at 3 weeks (P<.05). TEFF was not altered at 1 day and 1 week but decreased by 3 weeks (P<.05). MCE trended downward from baseline of 47+/-5%, reaching significance at 3 weeks (34+/-6%, P<.05). CONCLUSIONS: CEFF decreases acutely, indicating diminished economy of myocardial contraction. CEFF normalizes at 1 week, suggesting adequate compensation. TEFF is not altered in early AR. By 3 weeks, LV systolic dysfunction is accompanied by depressed TEFF, mechanical coupling, and CEFF signaling the onset of decompensated AR. Thus, volume overload of acute AR resulted in early compensation at the expense of myocardial efficiency with subsequent global dysfunction characterized by depressed LV systolic mechanics, mechanical, coupling, and contractile efficiencies.

Acute Disease↗

Prognosis in heart failure: is systolic or diastolic dysfunction more important?

The clinical syndrome of congestive heart failure can result from inadequate myocardial contraction (systolic myocardial failure), from pseudo-heart failure due to circulatory overload, or from failure of the ventricles to fill at low pressure (diastolic myocardial failure). The presence of systolic or diastolic heart failure is most precisely defined by an examination of left ventricular pressure-volume relations. Diastolic failure commonly coexists with systolic dysfunction. However, in many patients, diastolic dysfunction may exist alone or as the predominant physiologic disturbance. This is especially true in such common disease states as systemic hypertension and ischemic heart disease. Like systolic heart failure, diastolic failure results in significant morbidity and mortality. Diastolic heart failure may correlate better with prognosis for symptoms and survival than traditional indices of systolic function. The presence of predominantly diastolic dysfunction in large numbers of patients with the diagnosis of congestive heart failure has important therapeutic implications.

Diastole↗

Diagnosis and treatment of heart failure based on left ventricular systolic or diastolic dysfunction.

Data from large and small clinical trials reflect major differences in the pathophysiology, treatment, and prognosis of left ventricular (LV) systolic and diastolic dysfunction. These studies also indicate that medical therapy can benefit patients with LV dysfunction regardless of whether or not they are symptomatic. Because the descriptive term congestive heart failure does not provide for these important distinctions, a new classification of LV dysfunction has been developed in which patients with LV dysfunction are categorized on the basis of normal or abnormal systolic function. This classification is based on a simple assessment of LV function, it is applicable to patients without symptoms, and it reflects differences in treatment and prognosis. Those with clinically significant LV systolic dysfunction (ie, an LV ejection fraction < 40%) benefit from therapy whether or not they have symptoms of heart failure. Those with LV dysfunction and a normal LV ejection fraction (ie, diastolic dysfunction) also benefit from medical therapy. Annual mortality is higher in those with systolic dysfunction than in those with diastolic dysfunction, but within each of these categories mortality is higher in those with symptoms than in those without. This classification can be useful in the diagnosis and treatment of individual patients as well as in epidemiologic surveys designed to assess medical practice patterns.

Diastole↗

[Recovery process from myocardial stunning after transient ischemia: assessment with pulsed wave Doppler transmitral flow pattern].

Sustained left ventricular systolic dysfunction after transient myocardial ischemia is well known as "myocardial stunning", but little is known about the recovery in left ventricular diastolic function. Changes in left ventricular systolic and diastolic performance following dobutamine-induced ischemia were investigated in 13 patients with chest pain syndrome and normal coronary arteries (control) and 34 patients with coronary artery disease. Two-dimensional echocardiography and pulsed wave Doppler transmitral flow velocity curves were recorded at baseline, after infusion of a peak dose of dobutamine and at 20 min and 2 hours after dobutamine infusion. In control subjects, left ventricular ejection fraction and the peak early diastolic filling velocity increased at the peak dose of dobutamine. At 20 min after the cessation of dobutamine infusion, these values were restored to the baseline levels. In patients with coronary artery disease, ejection fraction and peak velocity increased at the peak dose of dobutamine but decreased at 20 min after infusion compared with baseline values despite the restoration of heart rate and blood pressure. Although ejection fraction increased at 2 hours compared with 20 min after infusion, peak velocity did not increase. Left ventricular diastolic dysfunction may be sustained longer than systolic dysfunction after transient myocardial ischemia.

Aged↗

Subclinical hypothyroidism and cardiac function.

The cardiovascular system is sensitive to the action of thyroid hormone. However, although a wide spectrum of cardiac abnormalities has long been recognized in patients with overt thyroid dysfunction, the question of cardiac involvement in patients with subclinical thyroid dysfunction has been investigated only in the last two to three decades. Most clinical studies have shown that subclinical hypothyroidism or hyperthyroidism is associated with changes in several cardiac parameters. More specifically, the literature on cardiac involvement in subclinical hypothyroidism consistently shows that patients have resting left ventricular diastolic dysfunction evidenced by delayed relaxation, and impaired systolic dysfunction on effort that results in poor exercise capacity. Whether or not subclinical hypothyroidism also affects left ventricular systolic function at rest remains controversial. Studies of subclinical hypothyroid patients before and after euthyroidism was achieved with levothyroxine replacement provided evidence of impaired resting left ventricular systolic function. Indeed, at-rest left ventricular systolic function was substantially normal in most studies of subclinical hypothyroid patients compared to normal control subjects. Drawing on these data, it appears that subclinical hypothyroidism should be considered a mild form of thyroid failure, associated with initial signs of cardiovascular hypothyroidism. Therefore, it would seem appropriate to initiate timely treatment of patients with mild thyroid failure to prevent cardiac involvement.

Echocardiography, Doppler↗

The role of hypertension in the pathogenesis of heart failure. A clinical mechanistic overview.

Hypertension plays a key role in the evolution of the syndrome of heart failure. Hypertension has been identified as the chief precursor of left ventricular hypertrophy. Hypertensive left ventricular hypertrophy can lead to ventricular diastolic dysfunction; it is also a risk factor for myocardial infarction, which is a principal cause of left ventricular systolic dysfunction. Asymptomatic left ventricular dysfunction, whether systolic or diastolic, culminates in clinically overt heart failure when a threshold is exceeded or when other precipitating factors are superimposed. The onset of overt heart failure heralds a bleak outcome. These structural and functional changes associated with hypertension evolve over decades and are preventable with effective antihypertensive treatment. These observations emphasize the importance of early diagnosis and effective treatment of hypertension to prevent cardiac complications.

Heart Failure↗

Brain natriuretic peptide and left ventricular dysfunction in chagasic cardiomyopathy.

Global left ventricular (LV) systolic dysfunction is the strongest predictor of morbidity and mortality in Chagas disease. Echocardiography is considered the gold standard for the detection of LV dysfunction, but not always available in endemic areas where chagasic cardiomyopathy is most common. Brain natriuretic peptide (BNP) is a neurohormone that has been recently described as a simple and inexpensive diagnostic and prognostic marker for patients with congestive heart failure. Chagasic patients (n = 63) and non-infected healthy individuals (n = 18) were recruited prospectively and underwent complete clinical examination, echocardiography and 24-h Holter monitoring. BNP was measured from thawed plasma samples using the Triage BNP test. We observed high levels of BNP in association with depression of LV ejection fraction, with increase of LV end-diastolic diameter and with LV premature complexes. An elevated concentration of BNP, defined as a concentration of 60 pg/ml or more, had a sensitivity of 91.7%, specificity of 82.8%, positive predictive value of 52.4%, and negative predictive value of 98% for detecting LV dysfunction (LV ejection fraction < 40%).BNP measurement using a simple, relatively inexpensive and rapid test has a promising role in identifying LV dysfunction associated with chagasic cardiomyopathy. Equally important, patients with Trypanosoma cruzi infection who have low levels of BNP level in plasma have a very low likelihood of severe cardiac involvement, and echocardiography is probably not necessary.

Adult↗

[Role of left ventricular systolic and diastolic dysfunction in clinical manifestations of chronic heart failure in patients with prior myocardial infarction].

AIM: To study the impact of systolic and systolic dysfunction of the left ventricle (LV) on the clinical manifestations of chronic heart failure (HF) in patients with prior myocardial infarction (MI). MATERIALS AND METHODS: 102 patients (mean age 47.4 +/- 0.7 years) who had sustained large focal IM at least 6 months before were examined. LV echocardiography was made to define systolic-diastolic relationships in HF. RESULTS: Analyzing the prevalence of primary diastolic HF in patients with its different clinical manifestations, it may be concluded that LV diastolic dysfunction is of the leading pathogenetic value at early stages of ischemic heart dysfunction. A complex relationship between the clinical manifestations of HF and a number of parameters characterizing the systolic and diastolic function of LV was estimated by the multiple regression analysis and presented as a trinomial equation. CONCLUSION: The results of the regression analysis have shown that the clinical manifestation of HF intensifies as relaxation slows down and transmitral blood flow redistributes to the left atrial systole; the severity of HF also increases with the depletion of compensatory mechanisms responsible for LV contractility.

Diastole↗