Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Systolic Dysfunction”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 811 records · Page 45Linked to original sources

Subclinical cardiac dysfunction in sarcoidosis.

Clinically apparent myocardial disease is infrequent in sarcoidosis. However, autopsy data show myocardial involvement in up to 30 percent of patients. Unexplained exertional symptomatology is a common complaint in patients with sarcoidosis. In this study, we investigated whether abnormal cardiac function might limit exercise performance in patients with sarcoidosis without overt cardiac involvement. We studied exercise responses in 35 patients with sarcoidosis and compared them with 28 untrained controls. Seventy-seven percent of the patients were symptomatic. Pulmonary function test results were lower in the group with sarcoidosis than normal controls, but they were within normal range. Only one patient had evidence of ventilatory limitation to exercise. Sixteen (46 percent) patients had abnormally increased heart rates (HRs) at rest prior to exercise testing and/or with exercise. Rapid HRs were confirmed during daily activities by continuous ambulatory electrocardiographic (ECG) monitoring. Left ventricular ejection fraction (LVEF) was measured to determine if systolic dysfunction could account for abnormal HR responses. Of patients with abnormally increased HRs, five had LVEFs less than 50 percent, and eight had normal LVEFs, of whom 75 percent had tachycardia at rest. Retrospective comparison of HR responses and LVEF between patients who did or did not receive corticosteroids revealed no significant differences between groups. We conclude that abnormal HR responses in patients without evident cardiac sarcoidosis are common and exertional symptoms in this population are often associated with chronotropic abnormalities. The exact mechanisms underlying the chronotropic abnormalities are unclear, but they likely include ventricular systolic dysfunction, sinus node dysfunction from granulomatous infiltration, or combinations of the two.

Adult↗

Clinical relevance of retrograde inferior vena cava or hepatic vein opacification during contrast-enhanced CT.

OBJECTIVE: The purpose of this investigation was to explore the clinical relevance of retrograde inferior vena cava or hepatic vein opacification during contrast-enhanced CT. MATERIALS AND METHODS: We retrospectively identified 127 patients who underwent contemporaneous contrast-enhanced CT of the chest or abdomen and echocardiography. On CT, the presence of retrograde inferior vena cava or hepatic vein opacification and the rate of IV contrast injection (> 3 mL/sec, high; < or = 3 mL/sec, low) were recorded. On echocardiography, the presence of tricuspid regurgitation, pulmonary hypertension, or right ventricular systolic dysfunction was recorded. RESULTS: Retrograde inferior vena cava or hepatic vein opacification was more common in studies performed with a high rather than a low contrast injection rate (28/56 vs 6/71 patients, respectively; p < 0.01). This finding was 31% sensitive (5/16) and 98% specific (54/55) for right-sided heart disease at low contrast injection rates, and 81% sensitive (17/21) and 69% specific (24/35) at high injection rates. Multivariate logistic regression models showed that high injection rate, tricuspid regurgitation, pulmonary hypertension, and right ventricular systolic dysfunction were independent predictors of retrograde inferior vena cava or hepatic vein opacification (p < 0.05 for each). CONCLUSION: Retrograde opacification of the inferior vena cava or hepatic veins on CT is a specific but insensitive sign of right-sided heart disease at low contrast injection rates, but the usefulness of this classic sign decreases with high injection rates. This realization is important because many centers increasingly use high-injection-rate CT.

Adolescent↗

The role of ischemic mitral regurgitation in the pathogenesis of acute pulmonary edema.

BACKGROUND: Acute mitral regurgitation may cause pulmonary edema, but the pathogenetic role of chronic ischemic mitral regurgitation, a dynamic condition, has not yet been characterized. METHODS: We prospectively studied 28 patients (mean [+/-SD] age, 65+/-11 years) with acute pulmonary edema and left ventricular systolic dysfunction and 46 patients without a history of acute pulmonary edema. The two groups were matched for all baseline characteristics. Patients underwent quantitative Doppler echocardiography during exercise. Exercise-induced changes in the left ventricular volume, the ejection fraction, the mitral regurgitant volume, the effective regurgitant orifice area, and the transtricuspid pressure gradient were compared in patients with and without acute pulmonary edema. RESULTS: The two groups had similar clinical and baseline echocardiographic characteristics. They also had similar exercise-induced changes in heart rate, systolic blood pressure, and left ventricular volumes. In the univariate analysis, patients with recent pulmonary edema had a much higher increase than did the patients without pulmonary edema in mitral regurgitant volume (26+/-14 ml vs. 5+/-14 ml, P<0.001), the effective regurgitant orifice area (16+/-10 mm2 vs. 2+/-9 mm2, P<0.001), and the transtricuspid pressure gradient (29+/-10 mm Hg vs. 13+/-11 mm Hg, P<0.001). In the multivariate analysis, exercise-induced changes in the effective regurgitant orifice area (P<0.001), in the transtricuspid pressure gradient (P=0.001), and in the left ventricular ejection fraction (P=0.02) were independently associated with a history of recent pulmonary edema. CONCLUSIONS: In patients with left ventricular systolic dysfunction, acute pulmonary edema is associated with the dynamic changes in ischemic mitral regurgitation and the resulting increase in pulmonary vascular pressure.

Acute Disease↗

beta-adrenergic blockade in developing heart failure: effects on myocardial inflammatory cytokines, nitric oxide, and remodeling.

BACKGROUND: Whether beta-adrenergic blockade modulates myocardial expression of inflammatory cytokines and nitric oxide (NO) in heart failure is unclear. METHODS AND RESULTS: We administered oral metoprolol or no therapy to rats for 12 weeks after large myocardial infarction and subsequently examined left ventricular (LV) remodeling; myocardial tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6 expression; and NO. In untreated rats, echocardiography revealed significant (P<0.001) LV dilatation and systolic dysfunction compared with sham. Papillary muscle studies revealed isoproterenol hyporesponsiveness to be unaltered by NO synthase (NOS) inhibition. Circulating NO metabolites were undetectable. In noninfarcted myocardium, although inducible NOS (iNOS) mRNA was absent, TNF-alpha, IL-1beta, and IL-6 mRNA and protein were markedly elevated compared with sham (P<0.001), with 2-fold higher expression (P<0.025) of IL-6 compared with TNF-alpha or IL-1beta. Metoprolol administration starting 48 hours after infarction (1) attenuated (P<0.02) LV dilatation and systolic dysfunction, (2) preserved isoproterenol responsiveness (P<0.025) via NO-independent mechanisms, and (3) reduced myocardial gene expression and protein production of TNF-alpha and IL-1beta (P<0. 025) but not IL-6, which remained high. CONCLUSIONS: During heart failure development, adrenergic activation contributes to increased myocardial expression of TNF-alpha and IL-1beta but not IL-6, and one mechanism underlying the beneficial effects of beta-adrenergic blockade may involve attenuation of TNF-alpha and IL-1beta expression independent of iNOS and NO.

Adrenergic beta-Antagonists↗

Levosimendan: first in a new class of inodilator for acute and chronic severe heart failure.

Heart failure is the most common malignant disease in the developed world. Levosimendan (Simdax) is a novel intravenous agent that exerts inotropic effects through sensitization of myofilaments to calcium and vasodilator effects by opening ATP-dependent potassium channels on vascular smooth muscle. Infusion of levosimendan increases cardiac output due to an increase in stroke volume and heart rate, with a fall in pulmonary capillary wedge pressure. It has an active metabolite with a half-life of about 80 h, therefore infusions of 6 to 24 h result in hemodynamic effects that persist for 7 to 10 days. Preliminary observations suggest that a single infusion of levosimendan lasting 6 to 24 h in patients with severe heart failure due to left ventricular systolic dysfunction results in hemodynamic changes, symptomatic benefit and a reduction in morbidity and mortality over the following 2 to 4 weeks compared with placebo in one study and with dobutamine in another. Long-term follow-up suggests no loss of this early benefit over 6 months. Levosimendan is licensed for the treatment of decompensated heart failure in many countries but not in North America. Further large trials are being conducted comparing levosimendan with placebo and with dobutamine in patients with severe heart failure and left ventricular systolic dysfunction. If these studies confirm the benefits of levosimendan, then it may become routine therapy for the management of severe heart failure.

Cardiotonic Agents↗

Congestive heart failure and QRS duration: establishing prognosis study.

STUDY OBJECTIVES: There is a lack of epidemiologic information about duration of QRS complex in the general heart failure population. We sought to describe age, sex, and clinical subset specific prevalence of QRS prolongation in this population. METHODS: Data were abstracted from the Resource Utilization Among Congestive Heart Failure Study, which identified 29,686 patients with heart failure from a large, mixed-model managed-care organization during 1989 to 1999. A target population of 3,471 had echocardiographic data and ECG data obtained from automated sources during the first year of diagnosis. Systolic dysfunction was defined as heart failure plus a left ventricular ejection fraction < 45%. MEASUREMENTS AND RESULTS: Among the heart failure population, 20.8% of the subjects had a QRS duration > or = 120 ms. A total of 425 men (24.7%) and 296 women (16.9%) had a prolonged QRS duration (p < 0.01). There was a linear relationship between increased QRS duration and decreased ejection fraction (p < 0.01). A prolonged QRS duration of 120 to 149 ms demonstrated increased mortality at 60 months (p = 0.001), when adjusted for age, sex, and race (p = 0.001). Systolic dysfunction was associated with graded increases in mortality across ascending levels of QRS prolongation. CONCLUSIONS: Approximately 20% of a generalized heart failure population can be expected to have a prolonged QRS duration within the first year of diagnosis, suggesting that as many as 20% of patients with heart failure may be candidates for biventricular pacing.

Aged↗

[Diastolic function of the left ventricle in a North-African patient with homozygous sickle-cell anemia].

AIM: The aim of this study was to investigate left ventricular diastolic function in a group of homozygous Black African patients with sickle-cell disease via echocardiography-Doppler, and to describe the possible hemodynamic implications of these findings. PATIENTS AND METHODS: Fifty patients with sickle-cell anemia from two hematology departments in Yaoundé volunteered to participate in the study, carried out between May-October 1995. The presence of any other associated pathology (cardiovascular disorder, acute drepanocytic anemia, pregnancy) was excluded following a clinical, hematological and echocardiographic examination. A sex- and age-matched control group consisting of 50 healthy subjects was selected after the same examination criteria had been met. Mitral flow recorded by pulsed Doppler was measured, and the amplitudes of the E and A waves of the proto- and telediastolic flow, the E/A ratio, the decrease over time (DT) for the E wave, and the left ventricular isovolumetric relaxation time were also calculated. The limits of the confidence interval for the mean DT of the control group were used as the criterion to determine the following in the patient population: i) relaxation disorder profile, with DT > 154 ms; ii) restrictive disorder profile, with DT < 137 ms. RESULTS: The dimensions of the cardiac cavities and the left ventricular mass were higher in the patient population; 34 cases of left auricular dilatation (68%) and 33 cases of left ventricular dilatation 8 66%) were observed. In only two patients was a systolic dysfunction noted. The amplitudes of the mitral flow E and A waves were increased, and the DT was longer in the sickle-cell group. Forty patients (80%) had abnormal diastolic function, with a marked predominance of the 'relaxation disorder' profile (60%). The restrictive disorder profile was only observed in ten sickle-cell patients (20%), while ten others displayed a normal profile (20%). The means of the various clinical and echocardiographic parameters of the three categories of sickle-cell patients (based on their diastolic profile, i.e., normal, relaxation disorder, restrictive disorder) were compared. The clinical parameters could be superimposed in the 3 categories. The dimensions of the left auricle and the telesystolic diameter of the left ventricle were significantly larger in the restrictive disorder category. The latter category appeared to be more symptomatic, and included the two isolated cases of systolic dysfunction. CONCLUSION: Left ventricular diastolic dysfunction is commonly encountered in sickle-cell cases in the Cameroon. The restrictive disorder profile is less frequently observed, but appears to be more harmful at the hemodynamic level. The present results suggest that the study of diastolic function in patients with sickle-cell anemia could help identify hemodynamically at-risk subjects who require more specific cardiovascular care, even before a noticeable alteration in systolic function has taken place.

Adolescent↗

Behavior of circulating endothelin-1 in a group of patients with acute myocardial infarction.

The aim of this study was to investigate the behavior of plasma endothelin-1 (ET-1) in 23 patients with acute myocardial infarction, complicated and uncomplicated by left ventricular failure, and treated with and without thrombolytic agents. ET-1 was measured on admission; on days 2, 3, and 5; and again on discharge. In addition, on discharge, ET-1 was correlated with left ventricular systolic function. Left ventricular failure was present, on admission, in 14 patients, whereas the other nine did not have any hemodynamic impairment. On discharge, no patients had left ventricular failure, but 11 had moderate to severe left ventricular systolic dysfunction, defined as left ventricular ejection fraction (LVEF) < 40%. Fourteen subjects, matched for age and sex, served as a control group. Compared with the control range, ET-1 was highly elevated on the first day, in both uncomplicated (p < 0.01) and complicated patients (p < 0.001). Then it decreased rapidly in the uncomplicated group, reaching the control range within day 5, whereas in the complicated group it remained significantly elevated in comparison with both the control subjects and the uncomplicated patients, until discharge. ET-1 was not correlated with the peak of creatine-kinase MB isoenzyme in any group. In seven patients submitted to thrombolytic treatment ET-1 was always significantly lower than in the nonthrombolyzed patients (p < 0.05), but the pattern of variation across time was no different. On discharge, the difference in plasma ET-1 between patients with LVEF < 40% and the control group was significant (p < 0.001), as was the difference between patients with and without moderate to severe systolic dysfunction (p < 0.01). ET-1 was closely and inversely correlated with LVEF when patients were considered as a whole (p < 0.001). These results suggest that the ET-1 increase in the early phase of myocardial infarction could be due to an ischemic process, to stress reaction, and to cardiac hemodynamic impairment, and therefore, ET-1 may be a good marker of disease. In the following phase the ET-1, being correlated with LVEF, could be a reliable index of systolic function.

Aged↗

Pathophysiologic role of the renin-angiotensin-aldosterone and sympathetic nervous systems in heart failure.

PURPOSE: The pathophysiology of heart failure is reviewed, with particular focus on the role of abnormal neurohormonal activation of the sympathetic nervous system and the renin-angiotensin-aldosterone axis in the pathophysiology of this syndrome. SUMMARY: Events preceding myocardial infarction and heart failure are driven in part by norepinephrine, angiotensin II, and aldosterone. The sympathetic nervous system likely evolved to mediate acute regulation of the cardiovascular system, not the sustained activation that is seen in heart failure. Overexpression of beta1-receptors in animal models results in decreased left ventricular ejection fraction and ventricular remodeling. In patients with systolic dysfunction, beta-blockade has improved left ventricular function and decreased the risk of sudden death. Chronic exposure to excess angiotensin II produces eccentric ventricular hypertrophy, vasoconstriction, and sodium retention. Angiotensin-converting enzyme (ACE) inhibition causes only a transient depression of aldosterone concentrations; the chronic benefit from ACE inhibition in patients with heart failure likely results from augmentation of bradykinin and not from the inhibition of angiotensin II production. Administration of eplerenone, a selective mineralocorticoid receptor antagonist, following induction of ischemic injury in animals, blocked the progressive ventricular dilatation and reduction in systolic function observed in control animals; clinical studies indicate that those findings can be translated to human cardiovascular disease. Overactivity of the mineralocorticoid receptor in cardiomyocytes could be important even in the absence of excessive levels of aldosterone. Clinical studies demonstrated that strategies of neurohormonal blockade using an ACE inhibitor, angiotensin II receptor antagonist, and beta-blocker are ineffective in reducing circulating aldosterone in patients with heart failure caused by left ventricular systolic dysfunction. CONCLUSION: Aldosterone is a key deleterious hormone influencing all forms of cardiovascular disease, including hypertension, myocardial infarction, and heart failure. Treatment of many cardiovascular diseases should include specific antagonism of the adverse pathophysiologic consequences of aldosterone.

Angiotensin-Converting Enzyme Inhibitors↗

Neuropeptide Y, left ventricular mass and function in patients with end stage renal disease.

OBJECTIVE: Neuropeptide Y (NPY) is released during sympathetic stimulation and mediates the central effects of the adipostatic hormone leptin. The plasma concentration of NPY and leptin is increased in patients with end stage renal disease (ESRD), but it is unknown whether these substances are related to biochemical markers of sympathetic activity and to alterations in left ventricular (LV) mass and function in these patients. DESIGN: We investigated the relationship between NPY, norepinephrine (NE), leptin and echocardiographic measurements in a cross-sectional study in 198 patients with ESRD. RESULTS: NPY was directly related to plasma NE and heart rate but it was largely independent of arterial pressure and of retention of metabolic waste products. NPY was significantly higher in patients with LV hypertrophy and in those with LV systolic dysfunction than in those without these alterations. Of note, NPY emerged as an independent correlate of LV mass index and of LV ejection fraction (LVEF) (both P <or= 0.002) in multiple linear regression analyses including a series of cardiovascular risk factors. Furthermore in a multiple logistic regression model patients in the top NPY tertile had a risk for LV concentric hypertrophy that was 18.10 (95% confidence interval: 5.87-55.83) times higher than in those in the first tertile (P < 0.001). Leptin was unrelated to NPY as well as to LV mass and to systolic function. CONCLUSIONS: Elevated NPY is independently associated with LV concentric hypertrophy and systolic dysfunction in ESRD. It remains to be seen whether these links contribute to the high cardiovascular mortality in these patients.

Adult↗

Maximizing management of patients with decompensated heart failure.

Patients with decompensated congestive heart failure can be categorized into those with either acute or chronic presentations. Patients with acute decompensated heart failure most often have an acute injury that affects either myocardial performance (i.e., myocardial infarction) or valvular/chamber integrity (mitral regurgitation, ventricular septal rupture), which leads to an acute rise in left ventricular (LV) filling pressures resulting in pulmonary edema and dyspnea. Therapy for these patients is aimed at treating the underlying cause of the myocardial injury as well as pharmacologic strategies to reduce LV filling pressures and to improve cardiac performance. In contrast, the therapy of patients presenting with decompensated heart failure in the setting of chronic LV systolic dysfunction, treated with angiotensin-converting enzyme inhibitors, digoxin, diuretics, and may be beta blockers, represent a poorly defined clinical entity that lacks clear guidelines for treatment. These patients can present with symptoms of volume overload and/or low cardiac output without evidence for a volume overloaded state. Potential diagnostic and therapeutic approaches include (1) a pulmonary artery catheter for invasive hemodynamic monitoring, (2) intravenous inotropic therapy, (3) LV mechanical assist device therapy, and (4) cardiac transplantation. This review presents some of the advantages and disadvantages of each of these interventions for patients with chronic systolic dysfunction who present with decompensated symptoms and require specialized management in the hospital setting.

Acute Disease↗

Age-related differences in the use of cardiac medications in patients with coronary artery disease.

BACKGROUND: Benefits of aspirin and beta-blocker use in patients with coronary artery disease and angiotensin-converting enzyme (ACE) inhibitors in those with left ventricular systolic dysfunction are well documented in all age groups. OBJECTIVE: To investigate whether aspirin, beta-blockers, and ACE inhibitors are equally used in geriatric (> or =65 years) versus younger (<65 years) patients with coronary artery disease. SETTING: University-affiliated major academic hospital. METHODS: Records of 402 patients with coronary artery disease were analyzed for use of aspirin, beta-blockers, and ACE inhibitors. One hundred thirty patients with contraindications to use of these agents were excluded. RESULTS: Of 272 study patients, 85% were using aspirin and 71% beta-blockers. Among the patients with left ventricular systolic dysfunction, 79% were using ACE inhibitors. One hundred forty-seven patients were of geriatric age, whereas 125 were of younger age. No significant difference in the use of aspirin (82% versus 89%, P = 0.10), beta-blockers (71% versus 70%, P = 0.85), or ACE inhibitors (86% versus 69%, P = 0.13) was found between geriatric and younger patients. This lack of difference in use of cardiac medications between geriatric and younger patients persisted on gender-based subgroup analysis. On decade-of-age-based analysis, aspirin use was not equally distributed among all the decades of age (P < 0.005), but beta-blocker use was. CONCLUSION: Results of this study demonstrate equal use of aspirin, beta-blockers, and ACE inhibitors in geriatric versus younger patients with coronary artery disease. Aspirin use was not equally distributed among all the decades of age.

Adrenergic beta-Antagonists↗

B-type natriuretic peptide identifies silent myocardial ischaemia in stroke survivors.

OBJECTIVE: To test the hypothesis that B-type natriuretic peptide (BNP) predicts reversible myocardial ischaemia in stroke survivors who do not have chest pain or previous myocardial infarction. METHODS: 56 stroke survivors (mean (SE) age 68 (8) years) underwent tetrofosmin myocardial perfusion scanning with dipyridamole as the stressor. The degree of ischaemia was assessed by a scoring system (out of 64) by an experienced observer blinded to the results of BNP. RESULTS: In the whole cohort, BNP was significantly correlated with the degree of myocardial ischaemia on stress scanning (Spearman's r = -0.475, p < 0.001). BNP also correlated with the degree of reversible ischaemia (stress score - rest score; Spearman's r = 0.28, two tailed p = 0.049). In the cohort who did not have left ventricular systolic dysfunction (n = 44), BNP remained higher in patients with relevant myocardial ischaemia (mean (SE) BNP 20.9 pg/ml, 95% confidence interval (CI) 15.2 to 26.5 v 12.2 pg/ml, 95% CI 5.95 to 18.5; p = 0.046); 33 of the 44 patients had no chest pain or history of myocardial infarction. The relation between resting BNP and both inducible ischaemia and dipyridamole stress score remained significant (Spearman's r = 0.37 and -0.38, respectively). CONCLUSIONS: BNP correlates with the degree of reversible myocardial ischaemia in patients who do not have chest pain or a history of myocardial infarction or evidence of left ventricular systolic dysfunction. Stroke survivors with a high BNP deserve further investigations to rule out significant reversible myocardial ischaemia, in order to reduce their risk of cardiac death.

Aged↗

The value of NT-proBNP in early risk stratification of acute coronary syndromes.

INTRODUCTION: The N-terminal portion of brain natriuretic peptide (NT-proBNP) has been identified as an indicator of prognosis in different cardiovascular diseases. Its role in risk stratification in patients with acute coronary syndromes (ACS) is still under evaluation. OBJECTIVE: We aimed to evaluate the prognostic value of NT-proBNP measured in the first 48 hours after admission due to an acute coronary syndrome. METHODS: Our study included 142 patients (aged 62.7 +/- 12.0 years, 70.4% males) admitted to a cardiology unit with an ACS. All laboratory evaluations were performed in the first 48 hours after admission. The mean follow-up was 200 days. Death from any cause or hospitalization because of a major acute cardiovascular event (whichever occurred first) was defined as the end-point. RESULTS: Cardiovascular risk factors were found in a significant proportion of our sample (hypertension in 56.3%, diabetes mellitus in 38.0%, current or previous smoking in 51.4%, dyslipidemia in 67.6%). Fifty-eight patients had left ventricular systolic dysfunction (LVSD). Serum levels of NT-proBNP were 2174 +/- 4801 pg/ml. Variables associated with event-free survival in univariate analysis were: NT-proBNP (HR 1.007, 95% CI 1.003-1.011, for each 100 pg/ml increment), serum glucose (hazard ratio [HR] 1.007, 95% CI 1.001-1.012, for each 1 mg/dl increment) and maximum cardiac troponin I (cTnI) level (HR 1.005, 95% CI 1.001-1.009, for each 1 ng/ml increment). The white blood count (WBC) was marginally associated with a poor prognosis (HR 1.152, 95% CI 0.994-1.335, for each 1000/mm3 increment). After adjustment for the above variables, age, sex, left ventricular systolic dysfunction, diabetes, coronary anatomy and coronary revascularization using a forward likelihood ratio Cox regression model, NT-proBNP remained the only variable with significant prognostic value (HR 1.007, 95% CI 1.003-1.011, for each 100 pg/ml increment). CONCLUSIONS: These data suggest that NT-proBNP is a strong clinical predictor of prognosis in acute coronary syndromes. Its early measurement should be included in the risk stratification strategy in this setting.

Acute Disease↗

ACE inhibitors in heart failure: what more do we need to know?

ACE inhibitors have significantly decreased cardiovascular mortality, myocardial infarction (MI), and hospitalizations for heart failure (HF) in patients with asymptomatic or symptomatic left ventricular (LV) systolic dysfunction. Furthermore, the extended 12-year study of the SOLVD (Studies Of Left Ventricular Dysfunction) Prevention and Treatment trials (X-SOLVD) demonstrated a significant benefit with a reduction of cumulative all-cause death compared with placebo (50.9% vs 56.4%) [hazard ratio (HR) 0.86; 95% CI 0.79, 0.93; p < 0.001]. The survival benefits and significant reductions in cardiovascular morbidity related to treatment with ACE inhibitors are likely achieved by titrating the dose of ACE inhibitors to the target dose achieved in clinical trials. Although the ATLAS (Assessment of Treatment with Lisinopril And Survival) study, which randomly allocated HF patients to low- or high-dose lisinopril, showed no significant difference between groups for the primary outcome of all-cause mortality (HR 0.92; 95% CI 0.82, 1.03), the predetermined secondary combined outcome of all-cause mortality and HF hospitalization was reduced by 15% for the patients receiving high-dose lisinopril compared with low-dose (p < 0.001) with a 24% reduction in HF hospitalization (p = 0.002). Despite the use of ACE inhibitors, blockade of the renin angiotensin aldosterone system (RAAS) remains incomplete, with evidence of continued production of angiotensin II by non-ACE-dependent pathways. The safety and potential benefits of angiotensin receptor antagonists (angiotensin receptor blockers [ARBs]) in patients with impaired systolic function have been assessed in moderate to large clinical trials. In patients with impaired LV systolic function and HF, combination therapy with ARBs with recommended HF therapy including ACE inhibitors in patients who remain symptomatic may be considered for its morbidity benefit. Based on the CHARM (Candesartan in Heart failure: Assessment of Reduction in Mortality and morbidity)-Added data, candesartan cilexetil in addition to standard HF therapy results in a further reduction of cardiovascular mortality. Close monitoring of renal function and serum potassium levels is needed in this setting. The VALIANT (VALsartan In Acute myocardial iNfarction Trial) results suggest that valsartan is as effective as captopril in patients following an acute MI with HF and/or LV systolic dysfunction and may be used as an alternative treatment in ACE inhibitor-intolerant patients. There was no survival benefit with valsartan-captopril combination compared with captopril alone in this trial. Despite these results, ACE inhibitors remain the first-choice therapeutic agent in post-MI patients, and ARBs can be used in patients with clear intolerance. Although the use of ACE inhibitors may be appealing in patients with HF and preserved LV systolic function, there is currently no evidence from large clinical trials to support this.

Angiotensin II Type 1 Receptor Blockers↗

Clinical features of isolated ventricular noncompaction in adults long-term clinical course, echocardiographic properties, and predictors of left ventricular failure.

BACKGROUND: Isolated ventricular non-compaction (IVNC) is a rare disorder characterized by prominent trabecular meshwork and deep recesses. We retrospectively assessed the clinical characteristics and natural course of IVNC in adults diagnosed at our hospital. METHODS AND RESULTS: Sixty-seven adult patients (44 male, mean age 41 +/- 18 years) with the diagnosis of IVNC were evaluated in this retrospective cohort. Its prevalence was found to be .14%. Forty-seven patients (70%) had class I/II functional capacity. Fifty-seven patients (85%) had electrocardiographic abnormalities, and the most common one was left ventricular (LV) hypertrophy (25%). LV systolic function was depressed in 44 patients (66%), with a median ejection fraction (EF) of 35% (range: 20%-48%) at diagnosis. Multiple regression analysis revealed that age at initial presentation, the total number of affected segments, and the ratio of non-compaction/compaction (NC/C) were the independent predictors of LV systolic dysfunction. Familial occurrence of IVNC was 33%. During a mean follow-up of 30 months (range: 9-50 months), major complications including ventricular tachycardia, heart failure requiring hospitalization, and cerebrovascular events were observed in 36%, 34%, and 9% of the patients, respectively. Ten patients (15%) with IVNC died in this study. LVEF at initial presentation and functional capacity at last visit were found to be independent predictors of mortality. CONCLUSION: This study suggests that IVNC is a form of cardiomyopathy with higher prevalence and relatively better prognosis than previously reported. Age at initial presentation, ratio of NC/C, and number of affected segments seem to be major determinants of LV systolic dysfunction, while initial LVEF and last functional capacity predict mortality in this cohort.

Adult↗

Electrocardiography and Doppler echocardiography for risk stratification in patients with chronic heart failure: incremental prognostic value of QRS duration and a restrictive mitral filling pattern.

OBJECTIVES: This prospective study tested whether Doppler echocardiographic variables add incremental value to QRS duration in determining the prognosis of patients with chronic heart failure (CHF) and systolic dysfunction. BACKGROUND: Diastolic dysfunction frequently is observed in patients with CHF, but its prognostic impact relative to that of QRS duration is unknown. METHODS: A total of 193 patients with CHF and an ejection fraction <45% were enrolled prospectively. Echo measurements included left ventricular dimensions/volumes, ejection fraction, mitral early/late diastolic velocity ratio, deceleration time, and tissue Doppler mitral annular velocities. The mitral filling pattern was classified as either restrictive (RFP) or nonrestrictive. A cardiac event (cardiac death or urgent cardiac transplantation) was defined as combined study end point. RESULTS: During a follow-up of 385 +/- 270 days, 24 patients suffered an event (cardiac death, n = 21; urgent transplantation, n = 3). The RFP, QRS duration, left ventricular systolic diameter, and mitral annular early diastolic velocity were independent predictors of an event. In patients with QRS duration >144 ms, the outcome was markedly poorer in the presence of RFPs as compared with their absence. Similarly, despite a QRS duration <or =144 ms, the outcome was worse in the presence of a RFP. A risk-stratification model based on the three strongest independent predictors separated groups into those with good prognosis and those with high, intermediate, and low event-free survival rates. CONCLUSIONS: In subjects with CHF and systolic dysfunction, transmitral flow patterns add incremental value to QRS duration in determining the prognosis.

Chronic Disease↗

Central sleep apnea in congestive heart failure: prevalence, mechanisms, impact, and therapeutic options.

Heart failure due to left ventricular systolic dysfunction is a prevalent syndrome and associated with morbidity, mortality, and huge economic cost. According to reports from several laboratories, a large number of patients with heart failure have central sleep apnea. Central sleep apnea causes arousals and sleep disruption, alters blood gases, and increases sympathetic activity. The pathophysiological consequences of central sleep apnea could adversely affect left ventricular structure and functions and worsen prognosis of heart failure. Several treatment options, including use of nocturnal supplemental oxygen, positive airway pressure devices, and theophylline have been systematically studied and have been shown to improve central sleep apnea. Long-term studies, however, are necessary to determine the impact of therapy on natural history of left ventricular systolic dysfunction.

Comorbidity↗