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PubMed2001

[Biventricular impairment of diastolic function in acromegaly].

AIM: Left ventricle impairment is very common in acromegaly. Concentric hypertrophy and diastolic dysfunction are observed at an early stage. Late left ventricle dilatation with systolic dysfunction may appear. Few reports have studied right ventricle diastolic function. METHODS: Twenty-seven acromegalic patients were included. Biventricular diastolic function was assessed using Doppler-echocardiography. Possible associations with hormonal activity, evolution time of illness, hypertension, left ventricular hypertrophy and systolic impairment on echocardiography were studied. RESULTS: Fifteen patients showed left ventricular diastolic dysfunction, whereas thirteen patients showed right ventricular diastolic dysfunction. A good correlation was observed between E/A relation of both ventricles (r = 0.70; p < 0.01) and isovolumetric relaxation time (r = -0.60; p < 0.01). The right ventricular E/A relation correlated with left ventricular mass index and significance was almost achieved with the presence of hypertension. There was no statistical correlations between the right ventricular E/A relation and hormone values or evolution time of illness. The left ventricular E/A relation showed a significant association with left ventricular mass index, isovolumetric time index and evolution time of illness. There were no statistical association with hormone values. CONCLUSIONS: The high prevalence of right ventricular diastolic dysfunction observed in acromegaly suggests the presence of acromegalic myocardiopathy.

Acromegaly↗
PubMed2004

Exercise capacity and cardiac function assessed by tissue Doppler imaging in chronic heart failure.

OBJECTIVE: To examine the relation between longitudinal left ventricular function assessed by tissue Doppler imaging (TDi) and exercise capacity in heart failure. SUBJECTS: 153 patients with chronic heart failure from left ventricular systolic dysfunction (ejection fraction < 45%) and 87 age and sex matched controls. METHODS: Echocardiography was used to measure conventional indices of left ventricular systolic function. TDi was used to assess left and right ventricular longitudinal function by measuring mitral and lateral tricuspid annular velocities during the cardiac cycle. Velocities measured at each point were the systolic peak (S(m)) and the diastolic troughs (E(m) and A(m)), corresponding to passive and active (atrial) left ventricular filling. Each patient also underwent treadmill exercise testing with metabolic gas exchange measurements. RESULTS: Left and right ventricular TDi velocities were greater in controls than in patients. Left ventricular ejection fraction (LVEF) correlated with S(m) (r = 0.30, p = 0.0005), but not with E(m), A(m), or the E(m)/A(m) ratio. There were no significant differences between New York Heart Association (NYHA) functional class for any of the TDi variables. Right ventricular indices were not related to exercise capacity. Systolic myocardial motion measured by TDi correlated more closely with peak oxygen consumption (pVO2) (r = 0.35, p < 0.0001) than LVEF (r = 0.21, p < 0.02). The E(m)/A(m) ratio was not correlated with pVO2. In multiple regression, S(m) was the only left ventricular TDi variable to predict exercise capacity independently (p < 0.05). CONCLUSIONS: Exercise capacity and symptoms are poorly related to conventional measures of cardiac function and more closely correlated with indices of longitudinal left ventricular function as assessed by TDi.

Case-Control Studies↗
PubMed1995

Echocardiographic and Therapeutic Approach to Heart Failure in the Elderly.

In most elderly patients, cardiac failure is associated with multiple cardiac pathologies, and the most common underlying abnormality is ventricular systolic dysfunction with reduced ejection fraction. In patients without cardiac enlargement, diastolic dysfunction may be predominant and left ventricular ejection fraction may be normal. Echocardiography is particularly suitable to evaluate changes in cardiovascular function that accompany age either as changes in disease patterns or as changes resulting simply from aging. The effects of digitalis on systolic and diastolic dysfunction are briefly reviewed, as well as the effects of diuretics, angiotensin-converting-enzyme inhibitors, and anticoagulant drugs.

Journal Article↗
PubMed2004

Reduction of systolic and diastolic dysfunction by retrograde coronary sinus perfusion during off-pump coronary surgery.

OBJECTIVES: We evaluated the protective effects of retrograde coronary sinus perfusion to offset potential systolic and diastolic dysfunction (myocardial stunning) after temporary regional ischemia needed for off-pump coronary artery bypass grafting. METHODS: Twenty Yorkshire-Duroc pigs (31.8 +/- 3.9 kg) underwent 15 minutes of mid-left anterior descending coronary artery ischemia in the beating heart. In 8 pigs, no protective measures were used. In 12 pigs, an aorta-coronary sinus shunt (with conventional cannulas) allowed retrograde perfusion during temporary ischemia; in 6 of these pigs, no leakage to the right atrium was ensured. Regional endocardial contraction was measured with sonomicrometer crystals. Systolic dysfunction (impaired regional shortening), diastolic dysfunction (contraction extending into early diastole), and coronary sinus nitric oxide and endothelin-1 levels were recorded. RESULTS: Before ischemia, contraction did not extend into the diastolic interval. During ischemia, paradoxic bulging occurred in all hearts except in the occlusive coronary sinus shunt group (16% +/- 6% of baseline, P <.01). Sixty minutes after ischemia, systolic segment shortening recovered 36% +/- 24% without retrograde perfusion versus 56% +/- 20% and 61% +/- 14% with coronary sinus shunting (P <.05). Diastolic dysfunction (as percentage of diastolic time in contraction) was 38% +/- 16% in the nontreated group versus 22% +/- 22% and 9% +/- 9% (P <.05) after shunting and occlusive shunting, respectively. This correlated with a left ventricular end-diastolic pressure increase of 4 mm Hg in the ischemic group versus no change in the retrograde perfusion groups. Nitric oxide decreased 15% without shunting and increased 8% after occlusive coronary sinus shunting (P <.05). CONCLUSIONS: Retrograde coronary sinus perfusion during simulated off-pump coronary revascularization diminishes systolic and diastolic dysfunction. An aortic-coronary sinus shunt is a rapid, recognized approach that can improve myocardial muscle and endothelial safety during off-pump coronary artery bypass grafting.

Animals↗
PubMed2004

Right ventricular long-axis function in relation to left ventricular systolic function.

A decrease in left ventricular (LV) systolic function is accompanied by a decrease in maximal relaxation velocity in LV long-axis direction, but is it also accompanied by a decrease in right ventricular (RV) long-axis function? To study this 35 consecutive patients were examined by echocardiography. Ejection fraction (LVEF) and mitral annulus motion (MAM) were used as indices of LV systolic function and tricuspid annulus motion (TAM), that is the systolic shortening in RV long-axis direction, was used as an index of RV systolic long-axis function. In the same way the maximal relaxation velocity in LV long-axis direction, that is the maximal diastolic velocity of MAM (MDV MAM), has been suggested as an index of LV diastolic function the maximal diastolic velocity of TAM (MDV TAM) can be supposed to be an index of RV diastolic function measuring the maximal relaxation velocity in the RV long-axis direction. A significant positive correlation was found between MDV TAM and MAM (r = 0.64, P<0001) and LVEF (r = 0.54, P = 0.001) and between TAM and the two studied indices of LV systolic function, with the highest correlation to MAM (r = 0.68, P<0.001) and the lowest to LVEF (r = 0.57, P<0.001). Thus, a decrease in LV systolic function is accompanied by a decrease in both systolic and diastolic RV long-axis function, findings that probably are due to the close anatomical connection between the ventricles and to changes that occur in afterload of the RV secondary to LV systolic dysfunction.

Aged↗
PubMed2004

Cardiac abnormalities 15 years and more after adriamycin therapy in 229 childhood survivors of a solid tumour at the Institut Gustave Roussy.

The purpose of this paper was to determine the cardiac status in children 15 years or more after adriamycin therapy for a solid tumour. Of the 447 pts, 229 pts were fully studied and 218 were not. The following cardiac evaluations were proposed to all the 447 consecutive patients (pts): (1) cardiac Doppler US by one of two expert cardiologists; (2) cardiac rhythm and conduction abnormalities including 24-hour holter ECG; (3) (131)l-mlBG myocardial scintigraphy; (4) serum brain natriuretic peptide levels at rest; (5) an exercise test with VO(2) max measurement. The radiation doses delivered to 6 points in the heart were estimated for all patients who had received radiotherapy. Congestive heart failure was diagnosed in 24 of 229 (10%) evaluated pts, with a median interval of 15 years (0.3-24 years) from the first symptom after adriamycin treatment. Among the 205 remaining pts, 13 asymptomatic pts (6%) had severe (n=4) (FS<20%) or marked (n=9) (20< or =FS<25%) systolic dysfunction. In the 192 others, the median meridional end-systolic wall stress was 91 (53-135) and it exceeded 100 g cm(-2) in 52 pts. Using a Cox model, only the cumulative dose of adriamycin and the average radiation dose to the heart, were identified as risk factors for a pathological cardiac status. In conclusion, the risk of cardiac failure or severe abnormalities increases with adriamycin treatment, radiotherapy and time since treatment, even after a follow-up of 15 years or more. In our series, after an average follow-up of 18 years, 39% of the children had a severe cardiac dysfunction or major ventricular overload conditions. The risk increases with the dose of adriamycin and radiation received to the heart, without evidence for threshold.

Adolescent↗
PubMed1999

Latent left ventricular dysfunction in patients with mitral regurgitation: feasibility of measuring diminished contractile reserve from a simplified model of noninvasively derived left ventricular pressure-volume loops.

BACKGROUND: Assessment of left ventricular (LV) contractility in mitral regurgitation is difficult, and latent systolic dysfunction may be present despite conventional indexes being in the "normal" range. We sought to demonstrate the presence of latent LV dysfunction in mitral regurgitation by showing diminished contractile reserve with the use of simplified pressure-volume loops from noninvasively derived parameters. METHODS AND RESULTS: We performed exercise echocardiography in 72 patients with isolated mitral regurgitation, minimal or no symptoms, normal resting LV function, and no coronary disease who subsequently underwent uncomplicated valve repair and in 15 healthy subjects. Simplified pressure-volume loops were constructed and LV stroke work was estimated at rest and immediately after exercise. As pressures were estimated, the findings were confirmed with a validated numerical model to estimate stroke work in patients and control subjects. Patients had a higher stroke work than did control subjects at rest (1.45 +/- 0.39 vs 0.92 +/- 0.21 J, P <.001). Eighteen patients had LV dysfunction develop after surgery. Patients with postrepair dysfunction had a significantly lower exercise stroke work (1.79 +/- 0.69) than did patients without (2.28 +/- 0.84 J, P =.02), but there was no difference in resting stroke work (1.48 +/- 0.39 vs 1.44 +/- 0.4, P = not significant). Change in stroke work with exercise was higher in patients with normal postoperative function (0.84 +/- 0.59 J) and control subjects (0.59 +/- 0.36 J) than patients with postoperative dysfunction (0.31 +/- 0.55 J, P =.001). The numerical model confirmed the lower exercise stroke work and change in stroke work in patients with postoperative dysfunction. CONCLUSIONS: The clinical study and numerical model confirmed diminished contractile reserve in patients who had LV dysfunction develop after uncomplicated mitral valve repair. Diminished contractile reserve may be a preoperative marker of latent contractile dysfunction.

Cardiac Volume↗
PubMed2006

Heart failure in elderly patients.

Several structural and functional changes contribute to heart failure in elderly patients: an age dependent increase in sympathetic nervous activity, left ventricular wall diameter, myocardial fibrosis and apoptosis, micro- and macrovascular coronary sclerosis, aortic stiffness. As a consequence, diastolic, but also systolic heart failure is a frequent finding in elderly patients. The relation of systolic to diastolic heart failure is clearly shifted towards diastolic heart failure in elderly patients, especially in women. Mortality is increased with systolic dysfunction in elderly patients compared to younger heart failure patients. Mortality is less with diastolic dysfunction, but still higher compared to elderly without heart failure. In addition, morbidity is increased both with diastolic and systolic heart failure in elderly patients. Cognitive dysfunction is a frequent finding. After exclusion of specific cardiac and extracardiac reasons for dyspnoea, drug therapy of systolic heart failure in elderly is similar to younger patients. However, the physiological decrease of renal function and the more frequent renal impairment in elderly patients with heart failure needs to be considered. Guideline recommendations for drug therapy are based in most cases on studies conducted in younger systolic heart failure patients. A recent meta-analysis of randomized beta-blocker trials suggests improved survival with beta-blockers even in the elderly subgroup. Guidelines for the treatment of diastolic heart failure are available only recently. The term heart failure with normal left ventricular ejection fraction (LVEF) has been proposed instead of diastolic heart failure. Given the increased morbidity and mortality in elderly patients with heart failure and normal LVEF, therapy should include general measures, such as physical activity, weight reduction, volume restriction. Specific therapy includes optimal control of systolic and diastolic blood pressure, diuretics, nitrates, and frequency-control. However, randomized trials evaluating the efficacy of specific therapies in heart failure with normal LVEF are still missing.

Adrenergic beta-Antagonists↗
PubMed2005

The imbalance between coronary reserve and wall stress explains the severity of ventricular dysfunction in hypertension.

BACKGROUND: The pathophysiologic role of coronary reserve impairment in hypertensive cardiac dysfunction is still debated. Previously, we demonstrated that satisfactory coronary vasodilatation may coexist with ventricular systolic dysfunction. It is conceivable that coronary reserve might otherwise be inappropriate for enhanced myocardial oxygen demand and may thus affect cardiac performance negatively. HYPOTHESIS: Myocardial supply-demand imbalance contributes to the severity of ventricular dysfunction in hypertension (HTN). METHODS: Fractional shortening (%) and end-systolic stress (10(3) x dyn x cm(-2)) were determined using echocardiography, and coronary reserve was calculated using transesophageal Doppler echocardiography. Coronary reserve/stress (cm2 x dyn(-1)) was utilized as a measure of supply-demand. Groups NL (20 healthy subjects), HTN1 (15 patients, fractional shortening > or = 30), HTN2 (19 patients, 20 < or = fractional shortening < 30), and HTN3 (21 patients, fractional shortening < 20) were constituted. RESULTS: Compared with NL and HTN1, groups HTN2 and HTN3 had significantly (p < 0.05) greater end-systolic stress (NL = 72 +/- 16, HTN1 = 72 +/- 23, HTN2 = 143 +/- 32, HTN3 = 186 +/- 70). Coronary reserve was impaired in HTN3 alone (NL = 3.5 +/- 0.6, HTN1 = 3.4 +/- 1.0, HTN2 = 3.1 +/- 1.0, HTN3 = 2.6 +/- 1.1), but coronary reserve/stress was reduced in both HTN2 and HTN3 (NL = 50 +/- 12, HTN1 = 53 +/- 21, HTN2 = 22 +/- 7, HTN3 = 15 +/- 7). Stepwise regression analysis identified diastolic internal dimension, end-systolic stress, and coronary reserve/stress as independently associated with fractional shortening. CONCLUSION: The imbalance between supply-demand explains the severity of hypertensive cardiac dysfunction and adds information to cardiac enlargement and elevated wall stress.

Adult↗
PubMed2005

Relation of lower hematocrit to progression from asymptomatic left ventricular dysfunction to symptomatic heart failure (from the Studies of Left Ventricular Dysfunction Prevention trial).

The relation between hematocrit and progression from asymptomatic left ventricular (LV) systolic dysfunction to symptomatic heart failure (HF) was examined in 2,821 patients from the Studies of Left Ventricular Dysfunction Prevention trial. Patients in the lowest hematocrit quartile (hematocrit < or = 40%) were at increased risk for the development of HF symptoms (hazard ratio [HR] 1.79, 95% confidence interval [CI] 1.37 to 2.34), first HF hospitalization (HR 2.35, 95% CI 1.52 to 3.62), and death or the development of HF symptoms (HR 1.60, 95% CI 1.28 to 1.99) compared with patients in the highest hematocrit quartile (hematocrit > 46%).

Aged↗
PubMed1999

Evaluation of the hemodynamic relationship between the left atrium and left ventricle during atrial systole by pulsed tissue Doppler imaging in patients with left heart failure.

The objective of the present study was to evaluate the hemodynamic relationship between the left atrium (LA) and left ventricle (LV) during atrial systole in the presence of an elevated left ventricular end-diastolic pressure (LVEDP) and LV failure using pulsed tissue Doppler imaging (TDI). Fifty-three patients with LV systolic dysfunction and no regional LV asynergy were divided into 3 groups: relaxation failure group (RF, n=20) with a ratio of peak early diastolic to atrial systolic velocity of the transmitral flow (E/A) < or = 1; pseudonormalization group (PN, n=19) with 1 or =2. In addition, 20 normal patients (E/A > or = 1) were studied as a control group. The transmitral and pulmonary venous flow velocities were recorded by transesophageal pulsed Doppler echocardiography. The wall motion velocity patterns were recorded at the middle portion of the LV posterior wall (LVPW) and at the mitral annulus (MA) of the LVPW site in the apical LV long-axis view by transthoracic pulsed TDI. The LVEDP was significantly greater in the PN and RS groups than in the RF and control groups. The moan pulmonary capillary wedge pressure was greatest in the RS group. The percent fractional change of the LA area during atrial systole determined by 2-dimensional echocardiography was significantly lower in the RS group than in the PN group. The peak atrial systolic pulmonary venous flow velocity was significantly greater in the PN group than in the RS group. The peak atrial systolic motion velocity (Aw) at the LVPW was significantly lower in the PN and RS groups than in the RF and control groups. The Aw at the MA was significantly lower in the RS group than in the other groups. There was no significant difference in Aw between the LVPW and MA in the RS group, whereas Aw at the MA was significantly greater than that at the LVPW in the PN group. In conclusion, the measurements of Aw at the LVPW and MA can be used to noninvasively evaluate the hemodynamic relationship between the LA and LV during atrial systole in patients with LV failure.

Adult↗
PubMed2006

Effect of body mass index on left ventricular cavity size and ejection fraction.

Extreme obesity is known to be associated with left ventricular (LV) systolic dysfunction. The relation of lesser degrees of obesity and LV systolic function is controversial. This study assessed the relation between body mass index (BMI; weight in kilograms divided by height in meters squared) and the LV ejection fraction (EF) and volumes in 1,806 subjects with normal technetium-99m sestamibi myocardial perfusion imaging results. BMI was evaluated as a continuous and a categorical variable (normal >18.5 and <25, overweight > or =25 and <30, obese > or =30 and <35, and severely obese > or =35 kg/m(2)). The prevalence of an EF < or =50% was similar in normal, overweight, obese, and severely obese subjects. On univariate analysis, only severely obese women had mildly reduced LVEFs. LV end-diastolic and end-systolic volumes increased linearly from normal to obese men and women, respectively (each p <0.01). On multiple linear regression analysis (R = 0.5, p <0.001), BMI (p = 0.03) and diabetes (p <0.001) influenced the EF adversely, whereas age and female gender were protective (p <0.001). However, on gender-stratified analysis, diabetes, not BMI, independently predicted the EF in men and women. BMI remained an independent predictor of greater end-diastolic volumes in men and women (p <0.01) even after accounting for co-morbidities. In conclusion, mild obesity was associated with LV dilatation, but the LVEF was preserved even with severe obesity. Weight control may be recommended to reduce the incidence of obesity-related co-morbidities and their impact on adverse LV remodeling.

Adult↗
PubMed2001

Cardiomyopathy Caused by Antineoplastic Therapies.

The goals of care for patients at risk for cardiomyopathy induced by cancer treatment should include prevention, early diagnosis, treatment of subclinical cardiac dysfunction, prevention of disease progression, and prolongation of patient survival. Any strategy aimed to minimize the cardiotoxic effects of cancer treatment should maintain the treatment's antineoplastic efficacy. Successful therapy achieves the highest health-related quality of life that is defined by the balance between maximizing the efficacy of oncologic therapy and minimizing the toxicity of this therapy. Doxorubicin-induced cardiotoxicity can be reduced by limiting the overall cumulative dose. There is no specific treatment for cancer therapy-related cardiomyopathy, and symptomatic patients should receive standard treatments for congestive heart failure such as afterload reduction, beta-blockers, diuresis, and digoxin. Afterload reduction with angiotensin-converting enzyme inhibitors such as enalapril and captopril may be indicated in patients with elevated afterload and asymptomatic left ventricular dysfunction diagnosed by echocardiography. Beta-blockers may improve myocardial systolic dysfunction and may be useful in the treatment of cancer treatment-induced cardiomyopathy. Cardiac transplantation remains a viable option in patients with cancer treatment-induced end-stage heart disease.

Journal Article↗
PubMed2006

Cardiac functional and morphologic changes of renal allograft recipients in the early posttransplant period.

UNLABELLED: After renal transplantation there is a substantial alteration in cardiac morphology and functions. This prospective study was undertaken to observe changes in different cardiac parameters in early months after transplantation. PATIENTS AND METHODS: Twenty-two allograft recipients (primary disease glomerulonephritis) were evaluated in the immediate pretransplant period (0 month) and 1 and 3 months after transplantation by clinical and echocardiographic (M mode, 2D) evaluations. RESULTS: Pretransplant echocardiogram showed left ventricular hypertrophy (LVH) in 100% subjects, LV dilation in 52%, and systolic dysfunction in 18%. By the third month, significant differences in systolic blood pressure (SBP-161 +/- 16 to 133 +/- 26 mm Hg, P < .002); diastolic BP (DBP-101 +/- 9 to 86 +/- 11 mm Hg, P < .006), and hemoglobin level (Hgb-7.3 +/- 1.6 to 11.2 +/- 3.9 g/dL, P < .006) were evident. Echocardiography showed decreased left atrial diameter (LADd-41 +/- 5 to 35 +/- 3 mm, P < .001); left ventricular internal diameter (LVIDd-54 +/- 6 to 47 +/- 6 mm, P < .02); left ventricular muscle mass index (LVMI-379 +/- 114 to 248 +/- 58 g/m(2), P < .001); and left ventricular end diastolic volume index (LVEDVI-96 +/- 28 to 64 +/- 17 ml/m2, P < .002). Bivariate correlations showed positive associations of mean blood pressure (MBP) and serum creatinine with LVMI, LVEDVI, and negative association of hemoglobin with MBP, serum creatinine, LVMI, and LVEDVI. CONCLUSION: From these observations, we concluded that cardiac morphological parameters start improving in the early posttransplant period. Improvements in renal function, anemia status, and lower blood pressure showed strong associations with these changes.

Adolescent↗
PubMed2004

[Physiopathology of severe sepsis].

Regarding the definition. Severe sepsis associates an explosive inflammatory reaction and organ failure. It is secondary to bacterial, fungal or viral infection. It can be at the origin of acute circulatory failure (state of septic shock). Response of the organism to infection. The presence of certain components of the membrane of pathogenic agents induces the release of various mediators in cascade, notably cytokines. Toll-like receptors (10 cloned in humans) intervene in the detection of microbes and in the inherent and subsequently adaptive immune response. Immune paralysis. The release of pro-inflammatory mediators characterizes the initial phase of sepsis. Persistence of the latter provokes acquired immunodepression, related to an anti-inflammatory profile, and hence to a delayed decrease in hypersensitivity, an incapacity to cope with the infection and the onset of nosocomial infections. The role of the mediators. During sepsis, the cytokines are predominantly pro-inflammatory (TNF-alpha and notably IL-1beta) whereas others, produced concomitantly or subsequently, are predominantly anti-inflammatory (IL-10 in particular). In fact, the majority of the cytokines have multiple and intrinsic effects, they mediate immune defense but also pathological manifestations. Many other mediators intervene: coagulation or complement systems, contact system, breakdown products of the phospholipid membrane, arachidonic acid metabolites, free radicals and nitrous oxide. Endocrine and metabolic dysregulations. The concept of relative adrenal insufficiency and peripheral syndrome of resistance to glycocorticosteroids have led to hormone replacement therapy during septic shock. Acute insulin resistance has also been described. The role of the endothelium and coagulation. The endothelium plays a key part in the onset of vascular insufficiency during sepsis due to abnormalities in vasomotricity and thrombomodulation. The anticoagulant regulating system is perturbed; there is a decrease in protein C with inactivation of its active form, which has pro-fibrinolytic properties, and a decrease in antithrombin III. Regarding myocardial dysfunction During septic shock there is often severe left ventricular systolic dysfunction, sometimes also involving the right ventricle, largely under-diagnosed despite its severe prognosis, and associated with reduced or even collapsed heart rate.

Animals↗
PubMed2006

Drug therapy recommendations from the 2005 ACC/AHA guidelines for treatment of chronic heart failure.

OBJECTIVE: To review and discuss key aspects of the drug therapy recommendations in the American College of Cardiology (ACC)/American Heart Association (AHA) 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure (HF) in the Adult. DATA SOURCES: Data were obtained from the ACC/AHA 2005 Guideline Update for Chronic HF. English-language clinical trials, observational studies, and pertinent review articles evaluating the pharmacotherapy of chronic HF were identified, based on MEDLINE searches through January 2006. STUDY SELECTION: Articles presenting information that impacts the evidence base for recommendations regarding the use of various drug therapies in patients with chronic HF were evaluated. DATA SYNTHESIS: The ACC/AHA 2005 Guideline Update for HF provides revised, evidence-based recommendations for the treatment of chronic HF. The new guidelines are based on a staging system that recognizes both the development and progression of HF. Recommendations are provided for 2 stages of patients (A and B) who do not yet have clinical HF but are clearly at risk and 2 stages (C and D) that include patients with symptomatic HF. The guidelines continue to emphasize the important role of neurohormonal blockade with angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, beta-adrenergic blockers, and aldosterone antagonists. Based on recent trials, updated recommendations address the roles of combination therapy and the selective addition of hydralazine and isosorbide dinitrate. Along with specific drug recommendations, information on the practical use of various drugs is provided. Although the guidelines primarily focus on HF due to systolic dysfunction, general recommendations are also provided for patients with preserved systolic function. CONCLUSIONS: The ACC/AHA 2005 Guideline Update provides evidence-based recommendations for healthcare professionals involved in the care of adults with chronic HF. Recent clinical trial findings have further clarified the evolving role of neurohormonal-blocking drugs in the prevention and treatment of HF.

American Heart Association↗
PubMed1999

Effect of diltiazem on cardiac remodeling in rats assessed by Doppler echocardiography and mRNA expression.

The purpose of this study was to examine the effect of diltiazem on cardiac dysfunction and the change in cardiac gene expression after myocardial infarction in rats. On the first day after myocardial infarction, rats were randomly assigned to a diltiazem treatment (Dil, n = 7) or an untreated group (MI, n = 8). We then performed Doppler echocardiographic examinations on the rats and measured their hemodynamics at 4 weeks after myocardial infarction. Following these measurements, their cardiac mRNA was analyzed. Diltiazem decreased the mean aortic pressure and heart rate. Left ventricular end-diastolic pressure (LVEDP) and central venous pressure (CVP) increased to 18 +/- 2 mmHg and 5 +/- 1 mmHg (P < 0.01). Diltiazem reduced LVEDP to 14 +/- 1 mmHg (P < 0.05), but it did not change CVP. The weight of the right ventricle in MI was significantly larger than in the control rats (control, n = 7, 0.46 +/- 0.02 g/kg vs. MI, 0.81 +/- 0.06 g/kg; P < 0.01). The left ventricular end-diastolic dimension (LVDd) in MI increased to 8.8 +/- 0.3 mm (P < 0.01, control, 6.1 +/- 0.3 mm). Diltiazem prevented an increase in the weight of the right ventricle (0.69 +/- 0.03 g/kg, P < 0.05) and LVDd (7.7 +/- 0.2 mm, P < 0.05 to MI). The rats within MI showed systolic dysfunction, defined by a decreased ejection fraction (control, 67 +/- 2% vs. MI, 36 +/- 3%, P < 0.01), and diastolic dysfunction, defined by the E-wave deceleration rate (control, 13.4 +/- 1.6 m/s2 vs. MI, 30.4 +/- 3.4 m/s2; P < 0.01). Diltiazem significantly prevented systolic and diastolic dysfunction. The increases in beta-MHC, ANP, and collagen type I and III mRNAs in the noninfarcted left ventricle and right ventricle were significantly suppressed by treatment with diltiazem. alpha-Skeletal actin increased in MI, and alpha-skeletal actin was more increased with Dil. In conclusion, diltiazem prevents cardiac dysfunction and morphological change due to left ventricular remodeling after experimental myocardial infarction.

Actins↗
PubMed1997

[Alteration of myocardial viability and systemic ventricular dysfunction after Senning procedure].

After a Senning procedure for transposition of the great arteries (TGA), systolic dysfunction of the right ventricle (RV) is common. Pre and peroperative chronicale hypoxia may be the cause of this ventricular myocardial alteration. In order to detect abnormalities of myocardial viability and to study their relationship to RV function, the authors studied 41 patients (pts), 11.3 +/- 3 years after a Senning procedure. All patients underwent myocardial scintigraphy of the RV under basal conditions. 1 hour after injection of 1.5 mCi of Thallium 201. The RV ejection fraction (n = 41) and at peak effort (n = 25). Exercise ability and aerobic capacity were assessed by exercise testing (Bruce) with gas exchange measurement and compared with 41 normal matched subjects. The cardiorespiratory response to exercise was altered in the Senning group : duration of effort (10.5 +/- 2 vs 13.2 +/- 2 min; p < 0.0001), peak VO2 (33 +/- 5 vs 44.4 +/- 6 ml/min/kg; p < 0.0001), anaerobic threshold (6 +/- 1 vs 8.4 +/- 1.9 min; p < 0.05) were lower compared to controls. Abnormalities of RV viability were observed in 18/41 pts (44%), moderate in 12 cases and severe in 6 cases. Resting and exercise RVEF were significantly lower in patients with myocardial defects (45 +/- 5 vs 51 +/- 7%; p < 0.0005, and 49 +/- 9 vs 58 +/- 9%; p < 0.05 respectively). In conclusion, after the Senning procedure for TGA, scintigraphic abnormalities of the systemic ventricule are common and associated with an alteration of systolic function at rest and on exercise.

Adolescent↗