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PubMed2005

Effects of carvedilol on left ventricular diastolic function and chamber volumes in advanced heart failure.

AIM: Carvedilol treatment in chronic heart failure (CHF) demonstrated to reduce mortality and rehospitalisation, and improvement of cardiac systolic function with reduction of left ventricular volumes and remodelling. The effects of the drug on left ventricular (LV) filling are less studied. Systolic dysfunction is often associated to diastolic alteration, pseudonormal and restrictive filling pattern are related with poor prognosis. In this study we evaluated diastolic cardiac modifications during carvedilol therapy at early and long term in patients with advanced CHF and pseudonormal or restrictive filling pattern by echo Doppler method. METHODS: We studied 59 patients with severe but stable CHF (40 in class NYHA III and 19 in class NYHA IV) with both systolic and diastolic dysfunction due to idiopathic or ischemic cardiomyopathy. Group I (n=32) received preceding treatment plus carvedilol and Group II (n=27) continued standard therapy with ACE-inhibitors, diuretics, digossin and vasodilators. In all subjects were evaluated LV volumes mass and ejection fraction (EF). Therefore, we studied transmitral filling parameters: Early filling wave (E), atrial filling wave (A), E/A ratio, deceleration time of E (DT) and isovolumetric releasing time (IVRT) by echo Doppler method. RESULTS: After 4 months of therapy carvedilol group showed a significant increase of A wave (p<0.001) DT (p<0.0001) and IVRT (p<0.0001), and significant reduction of E/A ratio (p<0.0005) respect to Group II. Any significant changes were observed for volumes mass and EF. Transmitral Doppler measurements remained unchanged or further ameliorated at 12 months (A p<0.0005; DT p<0.00002; IVRT p<0.000004; E/A p<0.0008), we also observed E wave reduction (p<0.001) in Group I respect to controls. Besides, after 1 year of follow-up we observed a reduction of systolic volume (p<0.001) pulmonary pressure (p<0.0001) and consequent increase of EF (p<0.001) in group treated with beta-blockers. Multivariate analysis demonstrated that Doppler modification were minimally related to heart rate and blood pressure reduction. CONCLUSIONS: Carvedilol treatment improve diastolic function in CHF with severe diastolic impairment driving restrictive or pseudonormal filling pattern towards altered pattern at early time. These changes remained also after 1 year of therapy and appeared to precede increase of systolic function and improvement of emodynamic status.

Adrenergic beta-Antagonists↗
PubMed1985

Intact systolic left ventricular function in clinical congestive heart failure.

Clinical congestive heart failure (CHF) is traditionally associated wtih significant left ventricular (LV) systolic dysfunction. Over a 1-year period, 58 patients with CHF and intact systolic function (LV ejection fraction [EF] 62 +/- 11%) were identified. An objective clinical-radiographic CHF score was used to document the clinical impression. Based on radionuclide evaluation of peak filling rate, 38% of these patients were found to have a significant abnormality in diastolic function as measured by peak filling rate (less than 2.50 end-diastolic volume/s). An additional 24% of the patients had probable diastolic dysfunction with borderline abnormal peak filling rate measurements (2.5 to 3.0 end-diastolic volume/s). The disease states most frequently associated with CHF and intact systolic function were coronary artery disease and systemic hypertension. During a 3-month sampling period 42% of patients with clinical diagnosis of CHF referred to the nuclear cardiology laboratory were found to have intact systolic function; thus, intact systolic function is not uncommon in patients with clinical CHF. Abnormal diastolic function is the most frequently encountered mechanism for the occurrence of CHF. Definition of systolic and diastolic function appears relevant for development of optimal therapeutic strategies for the treatment of patients with CHF.

Adult↗
PubMed2002

Do diuretics and aldosterone receptor antagonists improve ventricular remodeling?

There is no evidence that loop diuretics improve ventricular remodeling in patients with heart failure. Aldosterone receptor antagonists, which have an effect on natriuresis and diuresis, especially in conjunction with an angiotensin converting enzyme-inhibitor, have been shown to improve ventricular remodeling in patients with left ventricular systolic dysfunction. The mechanisms for this beneficial effect and a reduction in death due to progressive heart failure seen in the randomized aldosterone evaluation study (RALES) is likely related to the effect of aldosterone receptor antagonism on myocardial collagen formation and ventricular hypertrophy. Further proof of this hypothesis should be forthcoming from the results of the Eplerenone Heart Failure Efficacy and Survival Study (EPHESUS) early in 2003 in which the aldosterone receptor antagonist eplerenone is being evaluated in patients with systolic left ventricular dysfunction post myocardial infarction.

Diuretics↗
PubMed1997

Echocardiography Doppler in pulmonary embolism: right ventricular dysfunction as a predictor of mortality rate.

To test the hypothesis that right ventricular (RV) systolic dysfunction at the time of diagnosis of pulmonary embolism (PE) is a predictor of mortality rate, 126 consecutive patients with PE were examined with echocardiography Doppler (ED) on the day of diagnosis. RV function was assessed by evaluation of wall motion on a four-point scale. The material was divided into two groups: group A (n = 56) with normal or slightly reduced RV function and group B (n = 70) with moderately or severely reduced RV function. The overall mortality rate was 7.9% in the hospital and 15.1% within 1 year. Four deaths occurred in group A and 15 in group B (p = 0.04). All in-hospital deaths (n = 10) occurred in group B (p = 0.002). The variables associated with mortality rate were RV dysfunction and cancer (in-hospital, p = 0.002 and 0.004; 1 year, p = 0.04 and < 0.001, respectively). Nine (7.1%) deaths (all in-hospital) were caused by PE. Five of these patients had advanced-stage cancer. The in-hospital mortality rate in patients without cancer was 4%, all from PE and all in group B. In conclusion, RV dysfunction when diagnosis of PE is established is associated with mortality rate. A strategy for risk stratification of patients with PE with ED may be of clinical usefulness.

Aged↗
PubMed1999

Echocardiographic features of primary, secondary and familial amyloidosis.

BACKGROUND: Currently recognized types of amyloidosis include primary, familial and secondary, each of which may affect the heart. There may be differences in the heart response to the deposition of amyloid fibrils in these three forms of the disease. MATERIALS AND METHODS: Over a period of 10 years (1985-95), 28 consecutive patients with primary, 11 with secondary and 17 with familial amyloidosis were studied at the Departments of Cardiology of Laiko and Hammersmith Hospitals. The diagnosis of amyloidosis was confirmed by biopsies of subcutaneous fat, rectum, kidney, bone marrow, gum or sural nerve. Diagnosis of cardiac involvement was based on typical electrocardiographic and echocardiographic findings. RESULTS: The left ventricular fractional shortening (%) was reduced in primary compared with familial or secondary amyloidosis (29.8 +/- 10.2 vs. 36.2 +/- 6.5 vs. 36 +/- 5.9, P < 0.05). The transmitral flow velocity pattern was compatible with abnormal relaxation in most patients in the three groups [primary 16 (57%), familial 11 (64. 7%), secondary 6 (54.5%), P = NS]. Right ventricular systolic dysfunction (right ventricular dP/dt < 220 mmHg s-1 or tricuspid annulus systolic excursion < 10 mm) was present in 8 (28.6%), 2 (11. 8%) and 0 patients. Patients with primary amyloidosis were followed up for 15 +/- 6 months. There were 12 deaths, and repeat echocardiography in the survivors revealed a significant deterioration of left ventricular systolic function (fractional shortening = 23.6% +/- 8.8%, P < 0.05 vs. baseline). CONCLUSION: Primary amyloidosis is characterized by more severe cardiac involvement than the familial or secondary amyloidosis and has an ominous course.

Adult↗
PubMed2002

Right ventricular cardiomyopathy in beta-thalassaemia major.

AIMS: To evaluate right ventricular function in patients with beta-thalassaemia major and congestive heart failure. Background In patients with beta-thalassaemia major a high incidence of cardiac involvement still exists despite improved prognosis with chelation therapy. Development of severe right heart failure is common and has been attributed to pulmonary hypertension secondary to lung haemochromatosis. However, the possibility of direct right ventricular myocardial involvement in the absence of significant pulmonary hypertension has not been adequately investigated. METHODS: Twenty-nine consecutively screened patients with beta-thalassaemia major and congestive heart failure were investigated by Doppler echocardiography, right ventricular first-pass radionuclide examination and cardiac catheterization. Haemodynamic data were obtained both before and after volume loading. A control group of 39 patients with beta-thalassaemia major, free from cardiac disease, and matched for age, gender, body surface area and heart rate was used for comparison. A subset of the control thalassaemic group (n=15) underwent both radionuclide and haemodynamic assessment. RESULTS: The majority of patients were on non-optimal chelation therapy. Only two of 29 patients were found to have cor pulmonale. One other patient suffered from constrictive pericarditis. A restrictive filling pattern in both ventricles and left ventricular systolic dysfunction were evident in the other 26 patients. Pulmonary artery pressure (systolic, 33+/-8 vs 27+/-5 mmHg, P<0.05) and pulmonary vascular resistance (114+/-56 vs 65+/-29 dynes. s. cm(-5), P<0.01) were only mildly elevated in the heart failure group. After volume challenge, cardiac output remained unchanged although the increments of ventricular filling pressures were significant (Deltaright atrial: 4.8+/-2.2 mmHg, P<0.05; Deltapulmonary capillary wedge: 5.6+/-2.9 mmHg, P<0.05) and correlated with each other (r=0.69;P<0.001) in heart failure patients, suggesting pericardial constraint and ventricular interaction. In these patients compared with the control thalassaemic group, a lower right ventricular ejection fraction (29%+/-9 vs 59%+/-6, P<0.0001) without correlation with pulmonary artery pressures was found. Haemodynamically significant right ventricular dysfunction defined as mean right atrial pressure >10 mmHg and ratio of mean right atrial-to-capillary wedge pressure >0.8 was evident in 15 of the 26 patients (58%), all with severe symptoms, representing three fourths of the patients in functional class III and IV. Simultaneous pressure recordings in six of these 15 patients showed equalization of ventricular end-diastolic pressures within 5 mmHg. CONCLUSION: The majority of patients with beta-thalassaemia major and severe congestive heart failure demonstrated a unique haemodynamic pattern similar to that described in predominant right ventricular infarction, indicating severe right ventricular cardiomyopathy in addition to left ventricular dysfunction. The incidence of cor pulmonale as a cause of right heart failure seems to be much lower than previously hypothesized.

Adult↗
PubMed1993

Effects of long-term enalapril therapy on left ventricular diastolic properties in patients with depressed ejection fraction. SOLVD Investigators.

BACKGROUND: The aim of the present study was to analyze the changes in left ventricular diastolic function that occur in patients with chronic severe left ventricular systolic dysfunction in the absence or presence of prolonged therapy with an angiotensin converting enzyme inhibitor. METHODS AND RESULTS: Left ventricular function data (cineangiography plus Millar, frame-by-frame analysis) and right ventricular volumes (radionuclide angiography) were obtained at baseline and after an average follow-up of 12.4 months in 42 patients with a left ventricular ejection fraction of 35% or less. After baseline measurements, the patients were randomized to placebo (n = 16) or enalapril (10 mg BID, n = 26). In the placebo group, the changes in left ventricular function were characterized by increases in end-diastolic (159 +/- 43 to 170 +/- 44 mL/m2) and end-systolic (119 +/- 38 to 128 +/- 49 mL/m2) volumes accompanied by a downward and rightward shift of the diastolic pressure-volume relation. In contrast, decreases in end-diastolic (166 +/- 43 to 156 +/- 47 mL/m2) and end-systolic (125 +/- 43 to 111 +/- 42 mL/m2) volumes accompanied by a slight upward and leftward shift of the diastolic pressure-volume relation were noted in the enalapril group. These changes in left ventricular volumes were significantly different between groups (both P < .005) but were not attended by changes in left ventricular end-diastolic pressure, in time constant of isovolumic pressure decrease, or in right ventricular volumes. However, the chamber stiffness constant beta decreased from 0.044 +/- 0.027 to 0.032 +/- 0.019 mL-1/m2 in the placebo group, whereas it increased insignificantly in the enalapril group (0.040 +/- 0.028 to 0.041 +/- 0.028 mL-1/m2). These changes in chamber stiffness constant beta between baseline and follow-up were significantly different between placebo and enalapril groups (P < .05). Another index of chamber compliance, delta V/delta P, also confirmed the presence of opposite changes in left ventricular chamber compliance in the placebo group and in the enalapril group. The mean diastolic wall stress increased with placebo but not with enalapril (+51 versus -13 kdyn/cm2; P < .04) whereas left ventricular mass and the indexes of left ventricular sphericity tended to improve in the enalapril group. The changes in plasma levels of norepinephrine, atrial natriuretic peptide, and arginine vasopressin were, however, comparable in both groups. CONCLUSIONS: The data indicate that in patients with severe systolic left ventricular dysfunction, the progressive left ventricular dilatation was accompanied by a decrease in left ventricular chamber stiffness; enalapril therapy was able to prevent or partially reverse these changes and tended to reduce left ventricular mass and ventricular sphericity. Those changes were suggestive of partial reversal of left ventricular remodeling by enalapril administration.

Adult↗
PubMed2006

Effects of levosimendan on right ventricular function in patients with advanced heart failure.

Right ventricular (RV) dysfunction frequently complicates advanced left ventricular heart failure and contributes to an unfavorable prognosis. Levosimendan is a novel inodilator that beneficially affects hemodynamics and left ventricular systolic and diastolic function in patients with advanced heart failure. However, its effects on RV function have not yet been properly assessed in these patients. In this randomized trial, the impact of levosimendan or placebo on various echocardiographic parameters of RV systolic and diastolic function was investigated in 54 patients with advanced heart failure due to left ventricular systolic dysfunction. Tissue Doppler imaging maximal systolic tricuspid annular velocity (S wave) increased significantly only in the levosimendan group (8.2 +/- 3.2 vs 9.0 +/- 3.0 cm/s, p <0.03). Tissue Doppler imaging RV early diastolic velocity (E wave) and the ratio of early to late diastolic velocities (E/A) also increased significantly after levosimendan administration (p <0.01 and p <0.05, respectively). Systolic pulmonary arterial pressure decreased significantly (54 +/- 11 vs 43 +/- 11 mm Hg, p <0.01) in the levosimendan-treated patients. Levosimendan beneficially modulated neurohormonal and inflammatory status by decreasing B-type natriuretic peptide levels (p <0.05) and by altering the ratio of interleukin-6 to interleukin-10 in favor of the latter (p <0.05). In conclusion, levosimendan could offer further therapeutic advantages in patients with advanced heart failure by improving systolic and diastolic RV function.

Blood Pressure↗
PubMed2001

Maturation-dependent differences in regulation of sarcoplasmic reticulum Ca(2+) ATPase in sheep myocardium in response to pressure overload: a possible mechanism for maturation-dependent systolic and diastolic dysfunction.

We have previously demonstrated that pressure-overload hypertrophy in adult sheep is associated with myocardial dysfunction whereas that in young lambs is associated with normal contractility. To probe for possible mechanisms of these age-dependent differences, we assessed mRNA expression of genes encoding critical components of myocardial Ca(2+) handling in the same animal model. We studied left ventricular myocardium of young and adult sheep with short-term (48 h) and long-term (6 wk) pressure overload induced by ascending aortic constriction. Six weeks of pressure overload induced the significant left ventricular hypertrophy (36 and 39% increase in left ventricular/body weight ratio in lambs and sheep, respectively). The Ca(2+) ATPase and Na(+)/Ca(2+) exchanger mRNA decreased with pressure overload only in the adult (p < 0.05). Ca(2+) channel mRNA was slightly increased by pressure overload regardless of age (p < 0.05). Calsequestrin, sarcoplasmic reticulum Ca(2+) release channel, or myosin heavy-chain mRNA levels did not significantly differ. In adult sheep after 6 wk of pressure overload, decreases in load-adjusted midwall shortening (systolic dysfunction) and prolongation of relaxation time constant (diastolic dysfunction) correlated with decreases in Ca(2+)-ATPase mRNA. The sarcoplasmic reticulum Ca(2+)-ATPase protein level and Ca(2+) uptake activity of isolated sarcoplasmic reticulum vesicles were depressed only in the adult with pressure-overload hypertrophy but not in the young. We demonstrated age-dependent differences in mRNA expression of Ca(2+)-handling protein genes in response to pressure overload, which preceded the occurrence of hypertrophy and myocardial dysfunction. Thus, altered expression of Ca(2+)-handling protein genes may be one of the primary responses to pressure overload rather than a phenomenon secondary to myocardial hypertrophy.

Animals↗
PubMedDate not supplied

Care and management of the patient with right heart failure secondary to diastolic dysfunction: an advanced practice perspective and case review.

Until recently, most clinical trials associated with heart failure have studied systolic dysfunction. With the escalating geriatric population and dramatic increases in costs related to cardiovascular management regimens, more attention is being given to understanding diastolic failure induced by uncontrolled hypertension and cardiomyopathies. Researchers have demonstrated that the compensatory mechanisms associated with left ventricular diastolic dysfunction lead to elevated right heart pressures and eventually to right heart failure. When congestive heart failure is diagnosed, studies should be accomplished to differentiate between ventricular systolic or ventricular diastolic origins of the disease process, both to understand the origins of the heart failure and to guide clinical management. Therapy regimens and treatment goals must be directed toward controlling both systolic and diastolic pressures in order to achieve optimum outcomes.

Cardiovascular Agents↗
PubMed1986

Hemodynamic adaptation to acute myocardial contusion complicating blunt chest injury.

The immediate hemodynamic sequelae of blunt chest injury complicated by acute myocardial contusion were examined in multiply traumatized patients. Focal defects of ventricular wall motion defined by gated cardiac scintigraphy identified acute myocardial contusion in 28 of 43 patients, involving the right ventricle alone in 18 (group 1A), the left ventricle in 4 (group 1B) and both ventricles in 6 (group 1C). Qualitatively normal ventricular wall motion was found in the 15 patients (group 2). Although there was no difference between groups 1A and 2 in mean systemic oxygen transport (620 +/- 189 vs 627 +/- 105 ml/min/m2), left ventricular ejection fraction (52 +/- 14% vs 60 +/- 9%) or calculated left ventricular end-diastolic and end-diastolic and end-systolic volumes, mean right ventricular (RV) ejection fraction was significantly lower in group 1A (29 +/- 9%) than in group 2 (47 +/- 7%, p less than 0.01). Concomitantly, evidence of RV systolic dysfunction was ml/m2) but not in group 2 (RV end-systolic volume, 50 +/- 21 ml/m2, p less than 0.05). RV stroke work was similar between the groups, and RV pump function was identical by virtue of a larger RV preload in group 1A (RV end-diastolic volume 143 +/- 63 ml/m2) than in group 2 (RV end-diastolic volume 93 +/- 26 ml/m2, p less than 0.05). Thus, use of the RV Frank-Starling mechanism in patients with traumatic RV contusion maintains RV pump function at a level similar to that in traumatized patients without acute myocardial contusion.

Adaptation, Physiological↗
PubMedDate not supplied

Management of heart failure and coronary artery disease in patients with chronic kidney disease.

Cardiovascular disease (CVD) is a major contributor to the mortality and morbidity of patients who suffer from chronic kidney disease (CKD). Heart failure and ischemic heart disease (IHD) are both highly prevalent in this population. The diagnosis of myocardial dysfunction is usually based on echocardiography. As in the general population, systolic dysfunction is treated with a combination of diuretics, renin-angiotensin system blockade, and beta-receptor antagonists. Diastolic dysfunction is best managed by eliminating the cause. Non-invasive tests for coronary artery disease (CAD) may be less reliable in patients with renal disease compared with nonuremic patients. Medical therapy of IHD in this population is generally similar to that for other patient groups, but surgical revascularization appears to carry a higher risk of complications with poorer clinical outcomes. The choice of revascularization procedure (coronary artery bypass grafting versus percutaneous transluminal angioplasty) should be based on the specific coronary anatomy of a given patient as well as a consideration of other comorbid factors.

Angioplasty, Balloon, Coronary↗
PubMed2005

Electrocardiographic abnormalities and uremic cardiomyopathy.

BACKGROUND: Progressive renal disease is associated with an increased risk of cardiovascular death, specifically sudden death. We investigated the link between uremic cardiomyopathy, QT interval and dispersal, and arrhythmias (by ambulatory ECG monitoring) in patients at different stages of progressive renal disease. METHODS: In a cross-sectional study we investigated 296 patients with nondiabetic renal disease (53 transplant recipients, 55 hemodialysis patients, and 188 throughout the range of chronic renal failure). Patients underwent echocardiography, ECG, and ambulatory blood pressure and ECG monitoring. RESULTS: Left ventricular mass was increased from the earliest stages of renal disease (near-normal renal function), the predominant pattern being eccentric left ventricular hypertrophy (LVH). There was a progressive increase in LVH with loss of renal function, so that more than 80% of patients on renal replacement therapy have LVH, the dominant pattern being concentric LVH. The prevalence of diastolic dysfunction increased in parallel with changes in left ventricular mass but systolic dysfunction and ventricular dilatation did not. Increased QT interval and QT dispersal were associated with poor renal function (maximal in dialysis patients), and were linked to LVH and other echocardiographic abnormalities. Arrhythmias were uncommon on ambulatory recording but were more common with poor renal function, in the presence of uremic cardiomyopathy, and increased QT interval and dispersal. CONCLUSION: LVH is present from the earliest stages of progressive renal disease. This, and other forms of uremic cardiomyopathy, is linked to increased QT interval and dispersal, and with minor rhythm abnormalities, providing a link with the high risk of sudden death in this population.

Adult↗
PubMed2001

Cognitive dysfunction as a major determinant of disability in patients with heart failure: results from a multicentre survey. On behalf of the GIFA (SIGG-ONLUS) Investigators.

Cognitive dysfunction is a frequent finding among older patients with left ventricular systolic dysfunction; however, the clinical outcomes of such a finding are unknown. Also, disability is a common condition in heart failure, poorly responding to commonly used cardiovascular medications. The association between cognitive dysfunction and disability was assessed in 1583 patients with heart failure, but without cerebrovascular disease, previous stroke, or Alzheimer's disease, who were enrolled during 2 years of a multicentre pharmacoepidemiology survey. The association between groups of variables (demographics, comorbid conditions, medications, and objective tests, including the Hodkinson abbreviated mental test) and functional disability (as indicated by need for intensive assistance in at least one of Katz' activities of daily living) was first analysed using separate age and sex adjusted logistic regression models. Those variables, significant at a p<0.1 level in these models, were simultaneously entered into an age and sex adjusted summary regression model. Among 1583 patients suitable for analysis, cognitive dysfunction (as detected by abbreviated mental test score <7) was detected in 265/461 disabled patients, and in 150/1122 independent subjects (p<0.0001). According to logistic regression analysis, cognitive dysfunction was associated with disability (OR=6.49; 95% CI=4.39-9.59) after adjusting for potential confounders.Thus, cognitive dysfunction in patients with heart failure is independently associated with disability, which currently represents an overwhelming medical and financial problem to patients, caregivers, and public health services. As early recognition and treatment of low cardiac output states might reverse cognitive dysfunction, cost effective treatment for heart failure should include systematic diagnostic and therapeutic approaches to cognitive dysfunction.

Aged↗
PubMed2003

Doppler tissue analysis of mitral annular velocities: evidence for systolic abnormalities in patients with diastolic heart failure.

BACKGROUND: The presence of signs and symptoms of heart failure (HF), abnormal diastolic function and an ejection fraction > 45%, have been defined as diastolic HF (DHF). However, a cut-off value of 45% for ejection fraction seems arbitrary as mild systolic dysfunction may be overlooked. It was the goal of this study to assess the additive information derived from Doppler tissue imaging for patients with DHF. METHODS: As a measure of left ventricular (LV) long-axis function, systolic and diastolic velocities of the mitral annulus (peak, peak early, and peak late) derived from pulsed Doppler tissue imaging were assessed in 36 asymptomatic control subjects, 36 patients with DHF, and 35 patients with systolic HF (SHF). As a measure of overall LV performance, the Tei index (isovolumic contraction time and isovolumic relaxation time divided by ejection time) was assessed. RESULTS: In the DHF group, peak systolic annular velocity was reduced (7.1 +/- 1.2 cm/s) as compared with the control group (9.0 +/- 1.2 cm/s, P <.05), and was even lower in the SHF group (5.0 +/- 0.7 cm/s, P <.01 SHF group vs DHF/control groups). The Tei index was increased in the DHF group (0.53 +/- 0.14) in comparison with the control group (0.39 +/- 0.07, P <.05), and was highest in the SHF group (0.94 +/- 0.43, P <.01 SHF group vs control/DHF groups). Using peak systolic annular velocity < 7.95 cm/s as a cut-off value (derived from receiver operating characteristic curve analysis), patients with DHF were separated from control subjects with a sensitivity of 83% and a specificity of 83%. A Tei index > 0.43 separated patients with DHF and control subjects with a sensitivity of 79% and a specificity of 72%. CONCLUSION: Systolic long-axis LV function is also impaired in patients with DHF, resulting in feasible diagnosis of DHF by Doppler tissue imaging analysis of LV long-axis function and overall LV function with the Tei index.

Aged↗
PubMed2002

Recovery kinetics of oxygen uptake after cardiopulmonary exercise test and prognosis in patients with left ventricular dysfunction.

INTRODUCTION: The prognostic value of peak oxygen uptake (peak VO2) in patients with left ventricular systolic dysfunction is currently recognized and accepted. Some studies have shown that other cardiopulmonary exercise test (CPET) parameters have additional value. OBJECTIVES: To evaluate whether our population of patients with left ventricular dysfunction had similar results to those found by other investigators who showed that a slow normalization of oxygen uptake (VO2) during the recovery period of a CPET has prognostic value, and whether the recovery phase parameters have additional prognostic value to peak VO2 in these patients. METHODS: We studied 292 consecutive adult patients (81.5% male; mean age 52.4 +/- 10.6 years) with an ejection fraction below 40% (mean 23.6 +/- 8.8%) given their first symptom-limited CPET between 03/1993 and 08/2000. The etiology was ischemic heart disease in 154, idiopathic cardiomyopathy in 130 and other in 8 patients. NYHA class was I in 7%, II in 50.6% and III in 42.4% of the patients. Two years was defined as the maximum follow-up time; it was 551.5 +/- 242.2 days on average, and 62 events (death or cardiac transplantation) occurred. The following parameters were analyzed: peak VO2 (l/min and ml/kg/min), percent predicted peak VO2 (pred VO2) (l/min and ml/kg/min), VO2 every 15 seconds (sec) of the first 3 minutes of recovery (the difference between peak VO2/kg and VO2/kg every 15 sec in the recovery period (dif VO2), expressed in ml/kg/min, and also the time (sec) to reach 50% of peak VO2 (T1/2). It was considered that a combined end-point was reached if patients died or underwent cardiac transplantation. RESULTS: ROC curves of these parameters showed the following as cut-off values (area under the curve > 0.7) for the occurrence of events: peak VO2 < 60% of pred VO2, dif VO2 at 60 sec (< 3 ml/kg/min), 90 sec (< 5), 120 sec (< 8), 150 sec (< 8.6) and 180 sec (< 10.5) of the recovery and T1/2 > 115 sec. Survival analysis was performed considering pred VO2 < 60%, dif VO2 at 150 sec (the largest area under the curve) and T1/2 > 115 sec. In the survival analysis, when the decrease in VO2 at 150 sec was less than 8.6 ml/kg/min the number of patients with events increased from 9.2% to 43.5% (p < 0.001; log-rank), and when T1/2 was less than 115 sec the number of events increased from 12.3 to 34.2% (p < 0.001; log-rank). When the criteria of T1/2 and dif VO2 at 150 sec were considered together with pred VO2 < 60%, mortality increased from 31 to 54% and from 33 to 51%, respectively (p < 0.001, for both parameters; chi-square). CONCLUSIONS: A slow VO2 kinetics in the recovery period of the CPET by itself identified groups of patients with poor prognosis. The association of these parameters with peak VO2 enhanced the identification of groups at greater risk for events. A global evaluation of the CPET should be performed, considering other parameters besides peak VO2, particularly those related to VO2 kinetics in recovery (T1/2 and dif VO2 at 150 sec) as identified in this study.

Adolescent↗
PubMed2006

Early diastolic impairment of diabetic heart: the significance of right ventricle.

BACKGROUND: Left ventricular diastolic dysfunction represents the earliest preclinical manifestation of diabetic cardiomyopathy. Right ventricular function has not been studied in depth yet in diabetic patients, although the right ventricle has an important contribution to the overall cardiac function. This study was designed to assess diastolic and systolic ventricular function in both ventricles, in patients with type 1 diabetes, free from coronary artery disease and hypertension. METHODS: We studied 66 type 1 diabetic patients and 66 age- and sex-matched normal subjects by conventional and tissue Doppler echocardiography. A possible correlation was examined for age, diabetes duration and echocardiographic measurements of left ventricular and right ventricular functions with univariate analysis. RESULTS: Type 1 diabetic patients were found to have impaired diastolic function in both ventricles with either conventional or tissue Doppler echocardiography. On the contrary, systolic function in both ventricles was preserved in our diabetic population. The measured indexes showed an expected correlation with age and diabetes duration except from systolic velocity in tricuspid annulus determined by color tissue Doppler. Moreover, significant correlations were found among parameters of left and right ventricular function. CONCLUSIONS: Patients with type 1 diabetes mellitus have impaired diastolic function, and particularly relaxation, in both ventricles before the development of myocardial systolic dysfunction. These alterations in myocardial function may be attributed to ventricular interdependence as well as to the uniform effect of diabetes to cardiac function.

Adult↗
PubMed1998

Time-dependent changes in norepinephrine-induced left ventricular dysfunction and histopathologic condition.

BACKGROUND: Intense activation of the sympathetic nervous system or administration of high concentrations of catecholamines diminishes myocardial contractility and produces infarct-like lesions throughout the heart. This study was conducted to determine whether norepinephrine-induced left ventricular (LV) dysfunction reverses with time and whether the histopathologic condition and the cardiac dysfunction produced by high doses of norepinephrine are causally related. METHODS: Norepinephrine, 10 microg bolus followed by 2.5 microg/kg/min for 90 minutes, was administered to conscious New Zealand white rabbits. Control rabbits (n=8) received saline solution. LV function was evaluated either immediately (n=7), on day 4 (n=8), or on day 10 (n=7) after norepinephrine treatment. Transverse sections from the left ventricle were then prepared for light microscopic study. RESULTS: Animals studied immediately after norepinephrine treatment demonstrated severe LV dysfunction and a decrease in global LV compliance. In contrast, LV function and compliance were normal in rabbits studied on day 4, but tissue sections from the left ventricle showed diffuse areas of inflammation. By day 10 the inflammatory process had progressed, and substantial collagen deposition had occurred. LV systolic function was normal, but a decrease in LV compliance was evident at this time. CONCLUSIONS: The normal LV systolic function on days 4 and 10 in spite of multiple foci of inflammation suggests (1) that norepinephrine-induced LV systolic dysfunction is reversible and (2) that the histologic derangements and the LV dysfunction are not causally related.

Animals↗