[The clinical importance of myocardial vitality in chronic, postischemic left ventricular dysfunction].
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Chronic Disease↗
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Effect of statins and white blood cell count on mortality in patients with ischemic left ventricular dysfunction undergoing percutaneous coronary intervention.
BACKGROUND: While morbidity and mortality were shown to be increased in the setting of an elevated white blood cell (WBC) count for patients with acute coronary syndrome, the impact of statin therapy on mortality for patients with an elevated WBC count is unknown in high-risk patients with coronary artery disease. HYPOTHESIS: The goal of this study was to determine whether statin therapy improved survival in patients with elevated WBC count undergoing percutaneous coronary intervention (PCI) with preexisting left ventricular (LV) dysfunction, a population at high risk for adverse outcomes. METHODS: We retrospectively evaluated consecutive patient procedures performed at our institution from 1996 through 1999. Patients had a technically adequate angiographic left ventriculogram with a calculated ejection fraction (EF) < or = 50%. Patients with prior coronary artery bypass graft were excluded. Mortality data were retrieved using the U.S. Social Security Death Index. Follow-up ranged from 3.5 to 6.5 years. Means are provided with +/- standard deviation, and p values < 0.05 were considered significant. RESULTS: Of the study population of 238 patients (average EF 39 +/- 9.8%, mean age 57.5 +/- 12 years, 68% men) 61% underwent PCI for a recent myocardial infarction, 68% received stents, and 65% were discharged on statins. Mean WBC count was 9,000 +/- 3,100 cells/mm3, with 28% of patients having a WBC > or = 10,000 cells/mm3. During follow-up, 27% of our population died. Patients with a WBC > or = 10,000 had worse survival than patients with WBC < 10,000 (1-year survival: 86 vs. 96%, p < 0.05; 3-year survival: 79 vs. 89%, p < 0.05). Survival was significantly improved in patients on statin therapy regardless of WBC count, but the greatest benefit tended to be in patients with WBC > or = 10,000 (WBC > or = 10,000; odds ratio [OR] 5.14, 95% confidence interval [CI] 1.44-19.0, WBC < 10,000; OR 2.79,95% CI 1.13-7.1). Proportional hazard regression analysis demonstrated that both statin therapy and WBC count predicted mortality. CONCLUSION: Patients undergoing PCI with LV dysfunction discharged on statins had improved survival regardless of WBC count, with a trend for greater improvement in patients with elevated WBC counts. In addition, WBC count predicts mortality in this high-risk population with LV dysfunction undergoing PCI.
Angioplasty, Balloon, Coronary↗
Myocardial work load is a major determinant of norepinephrine-induced left ventricular dysfunction.
This study was conducted to determine whether increased myocardial energy demand plays a role in norepinephrine (NE)-induced left ventricular (LV) dysfunction. A range of arterial pressure-heart rate (P-R) products (myocardial energy demand) was produced in both conscious and pentobarbital sodium-anesthetized rabbits with the same dose of NE (10 micrograms priming bolus plus 2.5 micrograms.kg-1 x min-1 for 2.5 h). After NE treatment, LV function was evaluated in vitro and found to be markedly diminished in the rabbits that had an elevated P-R product. In contrast, LV function was not significantly affected when the P-R product was maintained near control levels during NE treatment. In separate experiments, rabbit hearts were isolated and exposed to NE (10,000 or 50,000 pg/ml) for 2.5 h under low P-R product conditions. These hearts exhibited a dose-dependent decrease in LV function that was modest compared with that observed in rabbits that had elevated P-R products during in vivo NE treatment. Our results suggest that high concentrations of NE may cause modest degrees of LV dysfunction independently of increases in myocardial energy demand, but the LV dysfunction is exacerbated when myocardial energy demand is elevated.
Anesthesia, General↗
Hexarelin, a growth hormone secretagogue, protects the isolated rat heart from ventricular dysfunction produced by exposure to calcium-free medium.
The effect of hexarelin, a potent synthetic growth hormone (GH)-secretagogue, and of human GH were studied on the mechanical and metabolic changes elicited by the calcium-paradox phenomenon in isolated rat hearts submitted to 5 min Ca(2+)-depletion followed by reperfusion with reintegrated Ca(2+)medium. Hexarelin, (80 microg kg(-1)s.c.) administered to normal male young rats for 3 and 7-day, time-dependently antagonized the sudden increase in resting tension of the isolated perfused hearts upon Ca(2+)-repletion. The beneficial effect of hexarelin was particularly evident in the 7-day treatment. In this instance, ventricular contraction peaked at 30 +/- 2 mmHg (controls, 76 +/- 7 mmHg) and the recovery of left ventricular developed pressure (LVDP) was two times higher (P<0.001) than that recorded in controls (LVDP, 29 +/- 2 mmHg). Moreover, the release of creatine kinase into the heart effluent during Ca(2+)-repletion was reduced by 40% (P<0.001) as compared to controls. The protecting activity of hexarelin against the damage induced by calcium-paradox in the heart was apparently divorced from any stimulation of the GH/insulin-like growth factor (IGF) axis, since plasma and heart concentrations of IGF-1 were similar to those measured in control rats. In contrast to hexarelin, administration of GH (400 microg kg(-1) s.c.) for 7 days did not affect the mechanical and metabolic manifestations of calcium-paradox in the perfused rat hearts. Hexarelin (8 microg ml(-1)) perfused for 60 min through the hearts in recirculating conditions did not modify heart contractility and failed to prevent ventricular hypercontractility developed on Ca(2+)-readmission. In conclusion, the mode of action of hexarelin in protecting the rat heart from calcium-paradox events is presently unknown; it would seem, however, that only prolonged exposure to hexarelin makes myocardial cells competent to maintain cytoplasmatic electrolyte balance and to control of Ca(2+)gain, two functions that are impaired during the 'calcium-paradox' phenomenon.
Animals↗
Contractile state is the major determinant of functional outcome in patients with left ventricular dysfunction treated with enalapril.
Large-scale drug trials have focused primarily on mortality and morbidity and less on the functional state of the myocardium. A model was developed to assess myocardial contractile state in patients with left ventricular (LV) dysfunction and to address the questions of differences in function between patients with and without overt heart failure, effects of enalapril, and best predictors of functional outcome. Pressure-angiographic data were obtained from 16 patients with overt heart failure and 47 without heart failure. Repeat studies were conducted in 41 patients following 1 year's treatment with enalapril or placebo. Left ventricular silhouettes were divided into 18 segments to estimate regional ejection fraction, wall stress and myocardial damage (% myocardial damage). Contractile state was assessed and ranked by ejection rate-preload-afterload relationships and by a score method based on 10 myocardial and ventricular function parameters. End-diastolic and end-systolic volumes (EDV, ESV) were significantly greater (P < 0.001), ejection fraction (EF) lower (P < 0.009), % myocardial damage greater (P < 0.008) and contractile state more depressed in patients with overt heart failure. Changes in EDV and ESV (delta placebo vs delta enalapril) were significant (delta EDV, P < 0.003; delta ESV, P < 0.014). Directional shifts in the diastolic pressure-volume relationships with enalapril or placebo depended primarily on the basal contractile state and diastolic volume range. The best single predictors of post-treatment EF were the score index (a surrogate parameter for the contractile state) and ESV. Added benefits of enalapril include the prevention of further dilatation in patients with less depressed contractile state and delay in the onset of heart failure. Asymptomatic patients with LV dysfunction should also be considered for angiotensin converting enzyme (ACE) inhibitor therapy.
Blood Pressure↗
Relation of right ventricular free wall mechanical delay to right ventricular dysfunction as determined by tissue Doppler imaging.
Several well-established echocardiographic parameters used in the assessment of right ventricular (RV) performance, as well as tissue Doppler imaging (TDI) to investigate RV free wall mechanical events, were prospectively obtained from a heterogenous group of 20 patients with varying degrees of pulmonary hypertension (mean age 51 +/- 13 years; World Health Organization class average 2.8, mean pulmonary systolic pressure 78 +/- 24 mm Hg) and compared with similar data retrospectively obtained from 20 healthy volunteers (mean age 45 +/- 15 years). Patients with varying degrees of pulmonary hypertension had worse RV performance parameters than healthy volunteers (RV fractional area change 37 +/- 13% vs 52 +/- 5%, p < 0.0001; RV myocardial performance index 0.76 +/- 0.31 vs 0.29 +/- 0.11, p < 0.0001; and eccentricity index 1.41 +/- 0.57 vs 0.98 +/- 0.06, p < 0.005). Similarly, in these patients with abnormal RV performance, TDI showed statistically significant smaller peak longitudinal RV free wall strain (-21.5 +/- 9.0% vs -28.0 +/- 4.1%, p < 0.01) and significantly delayed time to peak strain (459 +/- 76 vs 388 +/- 29 ms, p < 0.0005) values than in healthy volunteers; a very strong correlation between RV mechanical delay and RV fractional area change (r = -0.89) was noted.
Adult↗
Endothelin receptor blockade reduces ventricular dysfunction and injury after reoxygenation.
BACKGROUND: Reoxygenation of hypoxic myocardium during repair of congenital heart defects results in poor ventricular function and cellular injury. Endothelin-1 (ET-1), a potent vasoconstrictor that increases during hypoxia, may suppress myocardial function and activate leukocytes. The objective was to determine whether administration of an endothelin receptor antagonist could improve ventricular function and decrease cardiac injury after hypoxia and reoxygenation. METHODS: Fourteen piglets underwent 90 minutes of ventilator hypoxia, 1 hour of reoxygenation on cardiopulmonary bypass, and 2 hours of recovery (controls). Nine additional animals received an infusion of Bosentan, an ET(A/B) receptor antagonist, (5 mg/kg per hour) during hypoxia and reoxygenation. RESULTS: Right and left ventricular dP/dt in controls decreased to 78% and 52% of baseline, respectively, after recovery (p < 0.05). In contrast, Bosentan-treated animals had complete preservation of RV dP/dt and less depression of LV dP/dt. Bosentan reduced the hypoxia and reoxygenation-induced elevation of ET-1 and iNOS mRNA at the end of recovery (p < 0.05). Bosentan-treated animals had diminished myocardial myeloperoxidase activity and lipid peroxidation compared with controls (p < 0.05). Myocardial apoptotic index, elevated by hypoxia and reoxygenation, was lower in the Bosentan-treated animals (p < 0.05). CONCLUSIONS: Endothelin-1 receptor antagonism improved functional recovery and decreased leukocyte-mediated injury after reoxygenation. The reduction in cardiac cell death might also improve long-term outcome after reoxygenation injury.
Animals↗
Enalapril prevents perpetuation of atrial fibrillation by suppressing atrial fibrosis and over-expression of connexin43 in a canine model of atrial pacing-induced left ventricular dysfunction.
UNLABELLED: Effects of enalapril on a canine model of atrial pacing-induced atrial fibrillation (AF) with rapid ventricular responses were determined. METHODS: Four weeks of atrial rapid pacing was performed on twenty-four beagles pretreated with placebo (Group I, n = 14) or enalapril 1 mg/kg (Group II, n = 10). Atrial effective refractory period (ERP), P-wave width, duration of AF, and left ventricular ejection fraction (LVEF) were evaluated every week. AF cycle length was determined by spectral analyses of fibrillation waves. Quantitative analysis of histology was added. RESULTS: After 4 weeks of pacing, P-wave width was longer in Group I than in Group II, and the duration of induced AF was significantly longer in Group I (59.6 +/- 66.3 seconds) than in Group II (3.6 +/- 3.4 seconds, P < 0.05). AF cycle length was longer in Group I than in Group II despite similar shortening of atrial ERP. Mean ventricular rate during rapid atrial pacing was not different between the two groups. LVEF similarly decreased in both groups. Interstitial fibrosis and expression of connexin43 was greater in Group I than in Group II (interstitial fibrosis, 9.2 +/- 8.4 versus 1.9 +/- 2.1%, P < 0.05; connexin43, 5.3 +/- 2.2 versus 1.1 +/- 1.1%, P < 0.05). CONCLUSIONS: Enalapril suppressed atrial pacing-induced AF with tachycardia-mediated cardiomyopathy by suppressing interstitial fibrosis, connexin43 over-expression and conduction delay.
Animals↗
Alteration in energetics in patients with left ventricular dysfunction after myocardial infarction: increased oxygen cost of contractility.
BACKGROUND: Although the use of inotropic agents to treat congestive heart failure (CHF) in patients with coronary artery disease has yielded short-term hemodynamic improvement, long-term mortality has shown less improvement. The loss of cardiac muscle as a result of infarction not only decreases the pumping ability of the heart but also leads to some dramatic changes in myocardial energetics. However, little is known about the mechanoenergetics of the heart in patients with left ventricular (LV) dysfunction after myocardial infarction. METHODS AND RESULTS: The present study was designed to compare by means of the Vo2-pressure-volume area relation (PVA, a measure of total mechanical energy) and Emax (LV contractility index), the incremental oxygen cost of contractility measured as nonmechanical energy per unit increment in contractility in patients with various kinds of LV dysfunction. We assessed Emax, Vo2, and PVA using conductance and Webster catheters under control conditions and during different rates of dobutamine infusion (3 and 6 micrograms x kg-1 x min-1) in 30 patients with coronary artery disease. Patients were divided into three groups according to LV ejection fraction (EF): 10 without LV dysfunction (EF>/= 60%), 10 with mild LV dysfunction (40% </= EF < 60%), and 10 with severe LV dysfunction (EF < 40%). Under control conditions, the Vo2-PVA relation was linear in each group. Contractile efficiency, the reciprocal of the slope of this relation, was comparable among the three groups. The oxygen cost of contractility in the severe LV dysfunction group was significantly greater than in the groups without and with mild LV dysfunction (0.022 +/- 0.014 versus 0.005 +/- 0.002 and 0.0012 +/- 0.005 mL O2 x mL x mm Hg-1 per beat, P <.05). CONCLUSIONS: These findings suggest that the alteration in mechanoenergetics in patients with severe LV dysfunction after myocardial infarction may result from the increased oxygen cost of excitation-contraction coupling rather than from a reduction in the efficiency of chemomechanical energy transduction.
Adult↗
Association between serum n-terminal pro-brain natriuretic peptide concentration and left ventricular dysfunction and extracellular water in continuous ambulatory peritoneal dialysis patients.
BACKGROUND: This study investigated the association between serum N-terminal pro-brain natriuretic peptide (NT-pro-BNP) levels and extracellular water (ECW%) and left ventricular (LV) dysfunction in continuous ambulatory peritoneal dialysis (CAPD) patients. METHODS: The study involved 30 stable CAPD patients: 14 males, 16 females; mean age 52 +/- 14 years; mean CAPD duration 34 +/- 12 months; 12 with diabetes mellitus (DM) and 18 non-DM. Serum NT-pro-BNP levels were determined using electrochemiluminescence immunoassay. Baseline echocardiography was performed using a Hewlett-Packard Sonos 1000 (Andover, Massachusetts, USA) device equipped with a 2.25-MHz probe, allowing M-mode, two-dimensional, and pulsed Doppler measurements. Left ventricular mass index (LVMI) was calculated according to the Penn formula. A multifrequency bioimpedance analyzer was used; ECW% was calculated as a percentage of total body water and was considered the index of volume load. RESULTS: (1) Serum NT-pro-BNP level, ECW%, LVMI, and LV ejection fraction in CAPD patients were 3924 (240 - 74460) pg/mL, 36.7% +/- 2.2%, 158 +/- 48 g/m2, and 60.5% +/-11.2%, respectively. (2) Patients were divided into three tertiles (10 patients each) according to their serum NT-proBNP concentration [1st tertile 1168 (240 - 2096), 2nd tertile 4856 (2295 - 20088), 3rd tertile 35012 (20539 -74460) pg/mL]. The tertiles did not differ significantly in terms of age, sex, presence of DM, body mass index, or PD duration. Patients in the 3rd tertile (highest serum NT-proBNP concentration) had the highest LVMI (126 +/- 45 vs 160 +/-41 vs 200 +/- 23 g/m2 for 1st, 2nd, 3rd tertiles, respectively) and the lowest LV ejection fraction (66% +/- 11% vs 62% +/-6% vs 55% +/- 9%). ECW% did not differ significantly between tertiles (35.5% +/- 2.0% vs 37.5% +/- 2.0% vs 36.5% +/-2.0%). (3) In CAPD patients, serum NT-pro-BNP levels correlated positively with LVMI (r = 0.628, p = 0.003) and negatively with LV ejection fraction (r = -0.479, p = 0.033). Serum NT-pro-BNP levels did not correlate with ECW% (r = 0.227, p = 0.25). (4) Stepwise regression analysis showed that LV ejection fraction (beta = -0.610, p = 0.015) and LVMI (beta = 0.415, p = 0.007) were independently associated with the serum NT-pro-BNP concentration. CONCLUSIONS: There was no link between ECW% and serum NT-pro-BNP concentration. Thus, serum NT-pro-BNP levels may not provide objective information with respect to pure hydration status in CAPD patients. In contrast, serum NT-pro-BNP levels were linked to LVMI and LV ejection fraction in CAPD patients. Therefore, while the serum NT-proBNP concentration might not be a useful clinical marker for extracellular fluid volume load, it appears useful for evaluating LV hypertrophy and LV dysfunction in CAPD patients.
Adult↗
Harmonic imaging with Levovist for transthoracic echocardiographic reconstruction of left ventricle in patients with post-ischemic left ventricular dysfunction and suboptimal acoustic windows.
BACKGROUND: Attempts to perform transthoracic 3-dimensional echocardiography (3DE) are often encumbered by poor definition of chamber borders in adult patients who have technically suboptimal acoustic windows. METHODS: To assess whether harmonic imaging (HI) and contrast agents can facilitate transthoracic 3DE assessment of the left ventricle, we used fundamental imaging (FI), HI alone, and HI coupled with the echo-enhancing contrast agent Levovist in 15 consecutive patients with post-ischemic left ventricular (LV) dysfunction and technically difficult windows. Dynamic 3DE image data sets were obtained at 5-degree angles (36 slices) from a transthoracic apical view. From these data a total of 240 myocardial segments were analyzed with the use of dynamic short-axis paraplane slices at basal, middle, and apical LV levels (standard 16 segment model). For border definition, each segment was scored in random sequence on the following scale by 2 independent investigators: 0 = not seen, 1 = suboptimal visualization, and 2 = well defined. RESULTS: Our results showed a significant increase in the number of well-visualized segments when harmonic mode combined with Levovist injection was compared with FI and HI alone. CONCLUSION: Harmonic imaging alone improves LV assessment by 3DE when compared with FI. Contrast imaging in which Levovist is added to HI further improves the capability of transthoracic tomographic 3DE in the visualization of LV myocardial segments. This could allow 3DE by transthoracic windows to be used more widely in adults for the evaluation of LV volume and function.
Adult↗
Detection of early right ventricular dysfunction in Chagas' disease using Doppler tissue imaging.
BACKGROUND: The involvement of the right ventricle (RV) in Chagas' disease is frequent. Although echocardiography plays an important role in noninvasive assessment of cardiac function, evaluation of RV is challenging because of the anatomic and functional complexity of this chamber. METHODS: To study early functional abnormalities in the RV, we selected 18 patients with Chagas' disease, no other disease, and a normal echocardiogram; and 12 normal individuals as a control group. All participants were submitted to Doppler tissue imaging and the parameters of systolic (systolic wave and regional isovolumic contraction time) and diastolic (early and late expansion waves) function were analyzed at the level of the interventricular septum and free wall of the RV. RESULTS: Regional isovolumic contraction time values showed a statistically significant difference between the 2 groups both in the RV free (P =.0003) and septal (P =.003) walls. With respect to diastolic function, we observed a significant difference between groups involving the early expansion wave (P =.014) and e/a ratio (P =.004) of the RV free wall. CONCLUSION: Doppler tissue imaging proved to be useful in early detection of RV dysfunction in Chagas' disease, with potential use in risk stratification of these patients.
Adult↗
Transient global left ventricular dysfunction in a localized myocardial infarction related to occlusion of the distal left anterior descending artery.
In some patients with acute myocardial infarction (MI), wall motion in the noninfarcted area declines globally despite localized myocardial damage. In most, an infarct-related lesion is the proximal part of the left anterior descending artery (LAD). Previous studies have reported that hypokinesis of remote myocardium may be related to multivessel disease, impaired coronary flow, or coronary flow reserve in nonculprit arteries. This report describes the case of a 53-year-old man who presented with severe global left ventricular (LV) dysfunction after an acute MI associated with distal LAD occlusion. Follow-up echocardiographic examination revealed nearly normalized LV function 5 days after the episode. We discuss a plausible mechanism of dysfunction of noninfarcted myocardium.
Angioplasty, Balloon, Coronary↗
Safety and efficacy of percutaneous transluminal coronary angioplasty in patients with left ventricular dysfunction.
The risks and long-term outcome after 845 elective percutaneous transluminal coronary angioplasties (PTCA) in patients with left ventricular (LV) dysfunction (ejection fraction less than or equal to 40%) were examined. Procedural results were compared with 8,117 consecutive procedures in patients with ejection fractions greater than 40%. The patients with LV dysfunction were older (63 vs 60 years, p less than 0.01), had a greater incidence of prior myocardial infarction (84 vs 45%, p less than 0.001), prior bypass surgery (39 vs 21%, p less than 0.001), 3-vessel disease (62 vs 33%, p less than 0.001), and class IV angina (48 vs 41%, p less than 0.01) than the control group. Angiographic success was lower (93 vs 95%, p less than 0.01), and overall procedural mortality was increased ( 4 vs 1%, p less than 0.001) in the study group. Emergency surgery rates were identical (2%). No significant difference was found in rates of nonfatal Q-wave myocardial infarction (2 vs 1%). At mean follow-up of 33.5 months, 15% of the patients with LV dysfunction required late bypass surgery, 27% underwent repeat PTCA, and 59% were angina free. Actuarial survival at 1 and 4 years was 87 and 69%, respectively. Cox regression analysis identified 3-vessel disease, age greater than or equal to 70 years, class IV angina and incomplete revascularization as correlates of long-term mortality. These data suggest that PTCA may be an effective treatment for coronary artery disease in patients with LV dysfunction.
Adolescent↗
Neurohumoral changes in patients with left ventricular dysfunction following acute myocardial infarction and the effect of nitrate therapy: a randomized, double-blind, placebo-controlled long-term study.
BACKGROUND: Several neurohumoral mechanisms involved in cardiovascular regulation are activated in the failing heart, but only limited information is available regarding the influence of long-term nitrate therapy. MATERIALS AND METHODS: This was a double-blind, randomized comparison of isosorbide-5-mononitrate (IS-5-MN), 60 mg given orally, once daily for 11 months to patients (n = 47) with left ventricular (LV) dysfunction following acute myocardial infarction (AMI). Forty-five patients received placebo. All patients received ramipril.Plasma natriuretic peptides (atrial [ANP] and brain [BNP] natriuretic peptide), epinephrine, norepinephrine (NEPI), antidiuretic hormone, aldosterone (Aldo), renin activity (PRA), substance P, neuropeptide Y-like immunoreactivity, calcitonin gene-related peptide, and vasoactive intestinal peptide were measured at baseline and at the end of the treatment period. Clinical, echocardiographic, and hemodynamic data were also obtained. RESULTS AND CONCLUSIONS: Chronic nitrate therapy does not significantly affect the neurohumoral status in patients with LV dysfunction after AMI, apart from a decrease in ANP. Some hormones are more closely associated with diastolic dysfunction/increased volume load (ANP and BNP) and others are more closely associated with systolic dysfunction (PRA, NEPI, Aldo). There is a temporal dissociation of these 2 groups of hormones 1 year post infarction: ANP and BNP decrease, whereas NEPI and Aldo show a slight increase. BNP levels do not reflect all important pathophysiologic mechanisms in heart failure. Consequently, the use of other neurohormonal factors than BNP for monitoring of heart failure therapy should be explored.
Adult↗
[Effects of carvedilol, atenolol and their combination with fosinopril on cardiac rhythm variability, clinicofunctional status and quality of life in patients with postinfarction left ventricular dysfunction].
AIM: To study effects of carvedilol and atenolol and their combination with fosinopril on heart rhythm variability (HRV, clinicofunctional status and quality of life in postmyocardial infarction patients with moderate chronic cardiac failure (CCF). MATERIAL AND METHODS: An 8-week randomized open study enrolled 50 male patients (mean age 55.7 +/- 1.58 years) with postinfarction CCF. They were divided into two equal groups. Group one received carvedilol (24.4 +/- 2.0 mg/day) followed by addition of fosinopril (2.5-40 mg/day). Group 2 received atenolol (44.1 +/- 5.1 mg/day) followed by fosinopril in the same dose as in group 1. RESULTS: A 4-week therapy with carvedilol and atenolol effectively corrected depression of HRV in both the group. Combined therapy with these beta-adrenoblockers and fosinopril improved impaired global left ventricular contractility, exercise tolerance, quality of life, relieved symptoms of CCF. CONCLUSION: Carvedilol, atenolol and their combination with fosinopril in patients with postinfarction CCF improve clinico-hemodynamic and functional status, raise HRV and quality of life.
Antihypertensive Agents↗
Clinical update: the role of angiotensin II receptor blockers in patients with left ventricular dysfunction (Part II of II).
Almost 5 million individuals in the United States have chronic heart failure (HF), which is increasing in prevalence. Angiotensin-converting enzyme (ACE) inhibitors are standard therapies for HF, although more than 10% of patients with HF are unable to tolerate these agents. Furthermore, ACE inhibitors may not provide complete blockade of the renin-angiotensin system (RAS) in the long term. Because angiotensin II receptor blockers (ARBs) may block the RAS more completely than ACE inhibitors and are better tolerated, several large-scale ARB trials have been performed exploring their potential role in treating patients with symptomatic HF and left ventricular systolic dysfunction. The Losartan Heart Failure Survival Study (ELITE II) demonstrated no significant differences in morbidity and mortality between the ARB losartan and the ACE inhibitor captopril among elderly patients with HF. The Valsartan Heart Failure Trial (Val-HeFT) demonstrated reductions in hospitalizations for HF with the ARB valsartan when added to standard HF therapy, with no effect on mortality. Both trials suggested a potential negative interaction between ARB and beta-blocker therapy. The Candesartan in Heart failure-Assessment of Reduction in Mortality and morbidity (CHARM) program demonstrated significant reductions in morbidity and mortality with the ARB candesartan in patients with HF due to systolic dysfunction, with or without ACE inhibitors and with or without beta blockers. Thus, the addition of ARBs to the treatment regimen of patients with symptomatic HF should be strongly considered.
Angiotensin II Type 1 Receptor Blockers↗
Transthoracic Doppler assessment of pattern of left ventricular dysfunction in hypertensive heart disease: combined analysis of mitral and pulmonary venous flow velocity patterns.
Although mitral flow velocity pattern changes with the progression of left ventricular (LV) diastolic dysfunction, it lacks predictive value in individual patients because of pseudonormalization in the presence of congestive heart failure and many physiologic and pathologic contributors to the mitral flow velocity pattern. To determine whether analysis of pulmonary venous flow velocity patterns complements the information obtainable from the mitral flow velocity patterns in the evaluation of patterns of LV dysfunction of hypertensive heart disease in individual patients, the ratio of the peak early diastolic filling velocity/peak filling velocity at atrial contraction (E/A ratio) in the mitral flow velocity pattern and the ratio of the peak systolic forward flow velocity (S)/peak diastolic forward flow velocity (D) (S/D ratio) in the pulmonary venous flow velocity pattern by the transthoracic approach were determined in 107 hypertensive patients with and without congestive heart failure. Age-related normal values of the E/A and S/D ratios were determined in 61 normal subjects and used to judge the normality or abnormality of the patterns. Results of the study indicate that (1) although an increased mitral E/A ratio is strongly indicative of heart failure with normal LV systolic function, the mitral E/A ratio is frequently within the normal range in hypertensive patients with heart failure; (2) association of decreased pulmonary venous S/D ratios with a normal mitral flow velocity pattern indicates the presence of heart failure as a result of LV systolic dysfunction that is usually observed at the most advanced pattern of LV dysfunction; (3) mild LV diastolic dysfunction is likely to exist in patients with normal E/A ratios if the pulmonary venous S/D ratio is higher than normal value; (4) predictive accuracy in the detection of LV systolic and diastolic dysfunction would be improved if both mitral and pulmonary venous flow velocity patterns rather than the mitral flow velocity pattern alone were analyzed. In conclusion, analysis of pulmonary venous flow velocity recordings improves accuracy and reliability of the Doppler assessment of LV systolic and diastolic dysfunction, particularly in individual hypertensive patients with normal mitral flow velocity patterns.
Adult↗