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PubMed1995

Stress-induced left ventricular dysfunction in silent and symptomatic myocardial ischemia during dobutamine stress test.

The extent and severity of dobutamine-induced left ventricular (LV) dysfunction with and without angina were evaluated in 105 consecutive patients with significant coronary artery disease and a positive dobutamine stress echocardiographic test, defined as new or worsening wall motion abnormalities during high-dose dobutamine stress (up to 40 micrograms/kg/min). Wall motion score (WMS) was derived using a 16-segment, 4-grade scoring method. The difference between stress and rest WMS (delta WMS) was derived as a global measure of stress-induced LV dysfunction. Typical angina occurred in 61 patients (58%) during the test. There was no significant difference between patients with or without angina with respect to age, gender, prevalence of previous myocardial infarction, multivessel disease, or number of diseased coronary arteries. Patients with angina had a higher prevalence of a history of angina before the test. Rest, stress, and delta WMS, number and distribution of ischemic segments, and number of segments with an increase in regional WMS of > or = 2 were not significantly different in patients with or without angina. ST-segment depression was more frequent in patients with angina (56% vs 29%, p < 0.05). Patients with (vs those without) ST-segment depression had a significantly higher number of ischemic segments with normal baseline contraction, an equal total number of ischemic segments, and a similar delta WMS. It is concluded that in patients with anatomically and functionally significant coronary artery disease, the amount of stress-induced LV dysfunction evaluated by dobutamine stress echocardiography is similar in patients with or without angina.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1994

Identification of viable myocardium in patients with chronic coronary artery disease and left ventricular dysfunction: role of magnetic resonance imaging.

Nineteen patients (16 men and 3 women, mean age 51 years) with previous anterior myocardial infarction and severe stenosis (> or = 90%) of the left anterior descending coronary artery were studied by magnetic resonance imaging (MRI) without and with contrast media to verify the capability of MRI in identifying viable myocardium in areas of severe systolic dysfunction. In corresponding left ventricular segments, a comparison was made between regional signal intensities (SI) determined on MRI images before and 4, 8, 12, and 30 minutes after administration of paramagnetic contrast media (gadolinium diethylenetriaminepentaacetic acid, 0.4 mmol/kg intravenously) and metabolic parameters determined by iodine 123 phenylpentadecanoic acid (IPPA) scintigraphy. The SI and the time of maximum postcontrast enhancement were analyzed by dividing the left ventricle into 11 segments. Each segment was classified as normal (group 1, n = 116), hibernating (group 2, n = 50), or necrotic (group 3, n = 43) on the basis of the IPPA washout rate (> 30%, 10% to 30%, and < 10%, respectively). Regional SI demonstrated significant differences in absolute values at 12 minutes (group 3: 1.62 +/- 0.58 vs group 1: 1.32 +/- 0.52, p < 0.01, and vs group 2: 1.34 +/- 0.48, p < 0.05) and at 30 minutes (group 3: 1.71 +/- 0.47 vs group 1: 1.21 +/- 0.55, p < 0.01, and vs group 2: 1.49 +/- 0.57, p < 0.05) and in temporal distribution. These results suggest that MRI has a potential role in differentiating viable from necrotic myocardium in patients with chronic severe systolic dysfunction.

Contrast Media↗
PubMed1987

Lipoxygenase inhibitor nafazatrom fails to attenuate postischaemic ventricular dysfunction.

The role of lipoxygenase activation in the genesis of postischaemic myocardial dysfunction was investigated in open chest dogs undergoing a 15 min occlusion of the left anterior descending artery followed by 4 h of reperfusion. Treated animals (n = 9) received nafazatrom, a potent lipoxygenase inhibitor, 10 mg.kg-1 orally 4 h before occlusion followed by intravenous boluses of 1.5 mg.kg-1 and 0.5 mg.kg-1 5 min before occlusion and 1 min before reperfusion respectively. Control animals (n = 10) received saline. No discernible haemodynamic effects were produced by the drug. Collateral flow to the ischaemic zone (radioactive microspheres) was 0.14(0.02) ml.min-1.g-1 in the control group and 0.16(0.05) ml.min-1.g-1 in the treated group. The size of the occluded bed as determined by postmortem perfusion was 25.5(0.8)% of the left ventricle in the control and 24.3(1.3)% in the treated group. Histological examination showed a decrease in neutrophil infiltration of the non-ischaemic myocardium and, to a lesser extent, of the reperfused myocardium in nafazatrom treated animals, suggesting lipoxygenase inhibition. Systolic wall thickening (an index of regional function) was assessed using an epicardial pulsed Doppler probe. The two groups exhibited comparable systolic thickening under baseline conditions. Though treated animals showed less dyskinesis during coronary occlusion (p less than 0.05), recovery of function was not enhanced over controls and in both groups the reperfused myocardium was still dyskinetic at 4 h. Thus nafazatrom failed to improve postischaemic ventricular dysfunction, suggesting that leukotrienes do not contribute importantly to this phenomenon.

Animals↗
PubMed2000

Underutilization and clinical benefits of angiotensin-converting enzyme inhibitors in patients with asymptomatic left ventricular dysfunction.

Despite evidence of therapeutic benefit of angiotensin-converting enzyme (ACE) inhibitors for congestive heart failure and asymptomatic left ventricular (LV) dysfunction, recent studies suggest that in heart failure patients, rates of ACE inhibitor usage in clinical practice remain low. In this study, the medical records of 107 patients with documented LV dysfunction were investigated for patterns of ACE inhibitor usage; 6-month and 1-year outcomes and event rates were evaluated. At index admission, 48% patients did not receive ACE inhibitor treatment, 32% were initiated on treatment, 19% continued on a prior regimen, and 1% were discontinued. Patients seen by a cardiologist were more likely to receive ACE inhibitor treatment (53% vs 35%, p = 0. 172), as were patients with histories of hypertension (60% vs 40%, p = 0.044) or myocardial infarction (56% vs 44%, p = 0.221). Significantly shorter hospitalizations (5.9 vs 9.5 days, p = 0.001) were noted for patients with on-going ACE inhibitor treatment compared with those receiving newly initiated treatment or no treatment. At time of hospital discharge, 102 patients were alive. Of 54 patients who received ACE inhibitors, 67% received an insufficient dose. At a 6-month follow-up, of 51 patients on ACE inhibitors, 23% died or were readmitted to hospital compared with 55% of nonusers (p = 0.001). At 1 year, this event rate was 31% among ACE inhibitor users versus 71% among nonusers (p < 0.0001). Bivariate and multivariate analysis revealed absence of ACE inhibitor use as the only significant variable associated with the event rate (p < 0.0011). Thus, about half of patients with asymptomatic LV dysfunction received ACE inhibitors; 2/3 of these did not receive a sufficient dose. ACE inhibitor usage increased with involvement of a cardiologist, presence of coexistent hypertension, or prior myocardial infarction. Ongoing ACE inhibitor therapy was associated with shorter hospitalizations and fewer hospital readmissions or deaths.

Adult↗
PubMed2002

Survival after aortic valve replacement for severe aortic stenosis with low transvalvular gradients and severe left ventricular dysfunction.

OBJECTIVE: We sought to assess whether aortic valve replacement (AVR) among patients with severe aortic stenosis (AS), severe left ventricular (LV) dysfunction and a low transvalvular gradient (TVG) is associated with improved survival. BACKGROUND: The optimal management of patients with severe AS with severe LV dysfunction and a low TVG remains controversial. METHODS: Between 1990 and 1998, we evaluated 68 patients who underwent AVR at our institution (AVR group) and 89 patients who did not undergo AVR (control group), with an aortic valve area < or = 0.75 cm(2), LV ejection fraction < or = 35% and mean gradient < or = 30 mm Hg. Using propensity analysis, survival was compared between a cohort of 39 patients in the AVR group and 56 patients in the control group. RESULTS: Despite well-matched baseline characteristics among propensity-matched patients, the one- and four-year survival rates were markedly improved in patients in the AVR group (82% and 78%), as compared with patients in the control group (41% and 15%; p < 0.0001). By multivariable analysis, the main predictor of improved survival was AVR (adjusted risk ratio 0.19, 95% confidence interval 0.09 to 0.39; p < 0.0001). The only other predictors of mortality were age and the serum creatinine level. CONCLUSIONS: Among select patients with severe AS, severe LV dysfunction and a low TVG, AVR was associated with significantly improved survival.

Adult↗
PubMed2004

[Congenital aortic valve stenosis with left ventricular dysfunction: effect of percutaneous valvuloplasty].

Two girls aged 6 and 15 years with severe congenital valvular aortic stenosis and left ventricular (LV) dysfunction underwent successful balloon aortic valvotomy (BAV). Both patients had severe symptoms at the time of initial evaluation. The electrocardiograms showed LV hypertrophy and cardiac enlargement (cardiothoracic ratio 0.7 and 0.65) was evident in the chest roentgenograms. Immediately after BAV, the aortic valve peak-to-peak gradients decreased from 60 to 8 mmHg and 120 to 30 mmHg respectively, the LV end-diastolic pressures decreased from 47 to 13 mmHg and 40 to 15 mmHg, the LV ejection fractions improved from 40 to 65% in the second girl. On follow-up (30 and 36 ms respectively), both patients were asymptomatic with normalization of LV function and without a change in the residual gradient a cross the aortic valve.

Adolescent↗
PubMedDate not supplied

Increased resting Tl-201 lung-to-heart ratio is associated with invasively determined measures of left ventricular dysfunction, extent of coronary artery disease, and resting myocardial perfusion abnormalities.

BACKGROUND: Stress lung thallium 201 uptake correlates with left ventricular (LV) dysfunction and extent of coronary artery disease (CAD). Although Tl-201 is used less commonly for stress imaging, dual-isotope stress and viability protocols continue to use Tl-201 for rest imaging. We sought to investigate the association between increased resting Tl-201 lung-to-heart ratio (LHR) and hemodynamic indices of LV dysfunction, indices of myocardial perfusion, and extent of CAD. METHODS AND RESULTS: Over a 1-year period, we identified 192 consecutive patients who underwent dual-isotope stress perfusion imaging and cardiac catheterization within 30 days, without interim events or revascularization. Resting LHR was measured, and its association with invasively measured hemodynamic parameters, extent of CAD, and indices of myocardial perfusion at rest and stress was examined. Increased resting Tl-201 LHR was weakly but significantly associated with lower LV ejection fraction (EF) (r = 0.209, P <.05), higher pulmonary capillary wedge pressure (r = 0.25, P <.005), and LV end-diastolic pressure (r = 0.215, P <.01) but not with pulmonary artery systolic pressure. Increased LHR was also weakly associated with rest perfusion abnormalities including the sum rest score (r = 0.271, P <.001) and number of abnormally perfused segments (r = 0.25, P <.001) bud did not correlate with stress perfusion indices or ischemic burden. The 76 patients (40%) with LHR greater than 0.5 were more likely to have LVEF lower than 40% and 3-vessel/left main CAD. CONCLUSIONS: Increased rest Tl-201 LHR is weakly associated with higher LV end-diastolic pressure and pulmonary capillary wedge pressure and lower LVEF. LHR is also associated with the extent of previously infarcted myocardium and may indicate the presence of 3-vessel/left main CAD.

Age Factors↗
PubMed1997

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

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

Aged↗
PubMed2002

Prognostic role of myocardial blood flow impairment in idiopathic left ventricular dysfunction.

BACKGROUND: Depressed myocardial blood flow (MBF) has been reported in dilated cardiomyopathy. The aim of this study was to investigate whether MBF impairment is an independent predictor of prognosis in patients with idiopathic left ventricular (LV) dysfunction. METHODS AND RESULTS: Sixty-seven patients (52 male, mean age 52+/-12 years) with different degrees of idiopathic LV systolic dysfunction (average LV ejection fraction, 0.34+/-0.10; range, 0.07 to 0.49) were prospectively enrolled. Thirty-four subjects (51%) had no history of heart failure symptoms at enrollment (NYHA class I). All patients underwent clinical and functional evaluation and a PET study to measure absolute MBF at rest and after intravenous dipyridamole. During a mean follow-up of 45+/-37 months, 24 patients had major cardiac events, including cardiac death in 8 and development or progression of heart failure in 16 patients. Multivariate regression analysis (Cox proportional hazards model) revealed heart rate (chi(2) 11.06, P<0.001), LV end-diastolic dimension (chi(2) 11.73, P<0.001), and dipyridamole MBF (chi(2) 11.04, P<0.001) as independent predictors of subsequent cardiac events. Dipyridamole MBF < or = 1.36 mL. min(-1). g(-1) was associated with an increase in the relative risk of death, development, or progression of heart failure of 3.5 times over other more common clinical and functional variables. CONCLUSIONS: The present study demonstrates that severely depressed MBF is a predictor of poor prognosis in patients with idiopathic LV dysfunction independently of the degree of LV functional impairment and of the presence of overt heart failure.

Coronary Circulation↗
PubMed1999

Effects of AT1-receptor blockade on progression of left ventricular dysfunction in dogs with heart failure.

The objective of the present study was to determine the effects of early long-term monotherapy with the angiotensin II AT1-receptor antagonist valsartan on the progression of left ventricular (LV) dysfunction and remodeling in dogs with moderate heart failure (HF). Studies were performed in 30 dogs with moderate HF produced by multiple sequential intracoronary microembolizations. Embolizations were discontinued when LV ejection fraction was 30-40%. Two weeks after the last embolization, dogs were randomized to 3 mo of oral therapy with low-dose valsartan (400 mg twice daily, n = 10), to high-dose valsartan (800 mg twice daily, n = 10), or to no treatment at all (control, n = 10). Treatment with valsartan significantly reduced mean aortic pressure and LV end-diastolic pressure compared with control. In untreated dogs, LV ejection fraction decreased (37 +/- 1 vs. 29 +/- 1%, P = 0.001) and end-systolic volume (ESV) and end-diastolic volume (EDV) increased (81 +/- 5 vs. 92 +/- 5 ml, P < 0.001; 51 +/- 3 vs. 65 +/- 3 ml, P = 0.001, respectively) after 3 mo of follow-up compared with those levels before follow-up. In dogs treated for 3 mo with low-dose valsartan, ejection fraction was preserved (37 +/- 1 vs. 38 +/- 2%, pretreatment vs. posttreatment) as was ESV but not EDV. In dogs treated for 3 mo with high-dose valsartan, ejection fraction decreased (35 +/- 1 vs. 31 +/- 2%, P = 0.02) and ESV and EDV increased in a manner comparable to those levels in controls. Valsartan had no significant effects on cardiomyocyte hypertrophy or on the extent of interstitial fibrosis. We conclude that, for dogs with moderate HF, early long-term therapy with the AT1-receptor blocker valsartan decreases preload and afterload but has only limited benefits in attenuating the progression of LV dysfunction and chamber remodeling.

Angiotensin Receptor Antagonists↗
PubMed2006

Cardiac inflammation contributes to right ventricular dysfunction following experimental pulmonary embolism in rats.

Acute right ventricular (RV) failure following pulmonary embolism (PE) is a strong predictor of poor clinical outcome. Present studies test for an association between RV failure from experimental PE, inflammation, and upregulated chemokine expression. Additional experiments test if neutrophil influx contributes to RV dysfunction. PE was induced in male rats by infusing 24 microm microspheres (right jugular vein) producing mild hypertension (1.3 million beads/100 g, PE1.3), or moderately severe hypertension (2.0 million beads/100 g, PE2.0). Additional rats served as vehicle sham (0.01% Tween 20, Veh). In vivo RV peak systolic pressures (RVPSP) increased significantly, and then declined following PE2.0 (51 +/- 1 mm Hg 2 h; 49 +/- 1, 6 h; 44 +/- 1, 18 h). RV generated pressure of isolated, perfused hearts was significantly reduced in PE2.0 compared with PE1.3 or Veh. MCP-1 protein (ELISA) was elevated 21-fold and myeloperoxidase activity 95-fold in RV of PE2.0 compared with Veh or PE1.3. CINC-1, CINC-2, MIP-2, MCP-1, and MIP-1alpha mRNA also increased in RV of PE2.0. Histological analysis revealed massive accumulation of neutrophils (selective esterase stain) and monocyte/macrophages (CD68, ED-1) in RV of PE2.0 hearts in regions of myocyte damage. Electron microscopy showed myocyte necrosis and phagocytosis by inflammatory cells. LV function was normal and did not show increased inflammation after PE2.0. Treatment with anti-PMN antibody reduced RV MPO activity and prevented RV dysfunction. Conclusions-PE with moderately severe pulmonary hypertension (PE2.0) resulted in selective RV dysfunction, which was associated with increased chemokine expression, and infiltration of both neutrophils and monocyte/macrophages, indicating that a robust immune response occurred with RV damage following experimental PE. Experimental agranulocytosis reduced RV, suggesting that neutrophil influx contributed to RV damage.

Animals↗
PubMed2004

Influence of valve prosthesis type on the recovery of ventricular dysfunction and subendocardial ischaemia following valve replacement for aortic stenosis.

BACKGROUND: Long-standing aortic stenosis (AS) causes significant progressive left ventricular (LV) dysfunction and may result in subendocardial ischaemia. Following aortic valve surgery, LV function may improve and this may be accompanied by reversal of ischaemia. There is debate about the differential effects of valve substitutes. METHODS: We studied 33 patients with significant AS and impaired LV systolic function. Patients underwent trans-thoracic Doppler echocardiography and 12-lead electrocardiography pre-operatively, prior to discharge from hospital and at 2.5 (range 1.5-3) years follow-up. RESULTS: Twenty patients received a stentless valve and 13 a stented valve. No patient had significant aortic regurgitation, other valvular disease or coronary artery disease. LV fractional shortening (FS) increased from 19+/-6% to 26+/-7% post-operatively and to 33+/-12% at follow-up in the stentless group (p<0.001). In the stented group, no significant change was seen in the post-operative FS, although it improved at follow-up and at this point did not differ from the stentless group. LV mass fell from 338+/-72 to 265+/-64 g post-operatively and to 170+/-77 g at follow-up (p<0.001) in the stentless group, whereas in the stented group a significant fall was seen only at follow-up (329+/-51 g pre-operatively, 304+/-68 g post-operatively, 166+/-28 g at follow-up, p=0.01). LV free wall excursion increased from 0.8+/-0.3 to 1.1+/-0.4 cm (p=0.05) and to 1.4+/-0.3 cm (p=0.02 compared with pre-operative values) in the stentless group. In the stented group, values were 1.0+/-0.4, 1.0+/-0.3 and 1.3+/-0.2 cm (p=0.05 compared with pre-operative) at the three time points, respectively. QRS duration fell from 113+/-36 ms pre-operatively to 99+/-12 ms at follow-up in the stentless group and from 117+/-28 to 99+/-19 ms in the stented group, p=0.01 for both comparisons. QT interval fell from 385+/-54 ms pre-operatively to 366+/-39 ms at follow-up (p=0.04) in the stentless group with no significant change in the stented group (387+/-52 and 375+/-33 ms, p=0.24). There was reversal of LV strain pattern in 11 (55%) of the stentless group and 6 (46%) of the stented group and normalisation of the inverted U wave in two thirds of patients. CONCLUSION: In patients with AS and severe LV dysfunction, there is a more rapid improvement in LV function following aortic valve replacement with a stentless prosthesis. Improvements in those receiving stented valves appear delayed, although there were no differences between the groups in LV function or mass at follow-up. Normalisation of LV free wall systolic behaviour, narrowing of the QRS complex and a reduction in the QT interval suggest that AS is associated with subendocardial ischaemia that reverses following valve replacement.

Aortic Valve↗
PubMed2005

Usefulness of positron emission tomography in predicting long-term outcome in patients with diabetes mellitus and ischemic left ventricular dysfunction.

We assessed the value of positron emission tomography to predict long-term outcome in patients with diabetes and ischemic left ventricular (LV) dysfunction. Circumferential profiles of nitrogen-13 ammonia (NH3) and fluorine-18 fluorodeoxyglucose uptakes were obtained in 61 patients who had diabetes and ischemic LV dysfunction. Patient profiles were compared with those from a normal database. NH3 and fluorine-18 fluorodeoxyglucose defect sizes and extent of perfusion-metabolism mismatch (percentage of myocardium with fluorine-18 fluorodeoxyglucose uptake minus NH3 uptake >2 SD above the normal difference) were determined. Patients were followed every 6 months. Over a mean follow-up of 4.3 years, cardiac death occurred in 52% of patients who underwent revascularization and 61% of those who underwent medical therapy (p = 0.69). No clinical or imaging variables predicted cardiac death in patients who underwent revascularization. In those who received medical therapy, mismatch in > or =3% of the left ventricle (risk ratio 4.0, p = 0.01) was the only multivariate predictor of cardiac death. Revascularization improved survival of patients who had mismatch of > or =3% at 4 years (p = 0.003) and at 8 years (p = 0.012) of follow-up. Patients who had mismatch > or =3% and ejection fraction <30% had the greatest improvement in survival with revascularization compared with medical therapy (p <0.0001). Revascularization also improved 4-year survival of patients who had NH3 perfusion defects of > or =25% of the left ventricle (p = 0.02). In conclusion, mismatch identifies medically treated patients who have diabetes and LV dysfunction, who are at high risk for cardiac death. Intermediate- and long-term survival of patients who have diabetes and mismatch may be improved with revascularization, and those who have significant mismatch and severe LV dysfunction have the greatest benefit.

Aged↗
PubMed1997

Determinants of functional capacity in chronic mitral regurgitation unassociated with coronary artery disease or left ventricular dysfunction.

Impaired functional capacity is common in patients with mitral regurgitation (MR), but the determinants of functional capacity in patients with normal left ventricular (LV) function are unclear. Forty patients with chronic, isolated, nonrheumatic MR with no coronary artery disease underwent exercise echocardiography with continuous expired gas analysis. Cardiac output and regurgitant stroke volume were measured at rest and immediately after exercise by pulsed-wave Doppler echocardiography. For controls, 17 healthy volunteers without MR were also studied. Patients achieved a significantly lower VO2max compared with controls (25.6 +/- 7.7 vs 31.7 +/- 7.7 ml/kg/min, p = 0.008). VO2max showed better correlations with exercise cardiac output than with cardiac output at rest in both patients and controls. Multiple linear regression identified exercise cardiac output (partial r = 0.65), patient age (partial r = -0.56), and gender as independent determinants of VO2max (multiple R = 0.85, p <0.001). Cardiac output at rest, LV ejection fraction, regurgitant stroke volume, and fraction were not significant determinants. With exercise, the regurgitant stroke volume increased in 13 patients and decreased in 27 patients. The former 13 patients had a significantly lower exercise cardiac output (7.4 +/- 2.5 vs 9.4 +/- 2.6 L/min, p = 0.026). Patients who stopped exercise due to dyspnea (n = 7) had a significantly lower exercise cardiac output and VO2max compared with those who stopped due to fatigue (n = 33), with no differences in resting or exercise regurgitant volume. Patients with an increase in LV end-systolic volume with exercise (n = 8) also had a significantly lower exercise cardiac output (6.9 +/- 1.9 vs 9.2 +/- 2.7 L/min, p = 0.037) and showed a trend toward a lower VO2max (21 +/- 7.5 vs 26 +/- 6.4 ml/kg/min, p = 0.07). In patients with chronic MR, exercise cardiac output is the major determinant of VO2max. Regurgitant volume and fraction are not related to functional capacity. Limitations in functional capacity in these patients may be more related to a diminished cardiac reserve than to a large regurgitant volume.

Anaerobic Threshold↗
PubMed1999

New primary prevention trials of sudden cardiac death in patients with left ventricular dysfunction: SCD-HEFT and MADIT-II.

Primary prevention of sudden arrhythmic death in patients with organic heart disease with poor left ventricular function and/or heart failure is currently a major challenge in cardiology. Amiodarone (with or without beta blockers) and the implantable cardioverter defibrillator (ICD) are considered the 2 major therapeutic tools to prevent sudden arrhythmic death in these patients. Two large trials have been launched to define the prophylactic benefit of the ICD or amiodarone on total mortality in patients that receive optimal heart failure and anti-ischemic treatment but remain at high risk of dying suddenly. The Sudden Cardiac Death in Heart Failure Trial (SCD-Heft) is designed to determine whether amiodarone or the ICD will decrease overall mortality in patients with coronary artery disease or nonischemic cardiomyopathy who are in heart failure New York Heart Association (NYHA) class II or III and have a left ventricular ejection fraction < 35%. The primary endpoint is total mortality; secondary objectives are comparison of arrhythmic and nonarrhythmic mortality and morbidity in the 3 arms as well as quality of life, cost-effectiveness, and incidence of episodes of ventricular tachyarrhythmias. The Multicenter Automatic Defibrillator Implantation Trial (MADIT) II is a follow-up study to the MADIT trial. It examines the prophylactic benefit in coronary artery disease patients with a left ventricular ejection fraction of < 30%, who have had at least 1 myocardial infarction but require no further risk stratification. MADIT II is a sequential design trial that compares ICD versus no ICD therapy. Programmed electrical stimulation to test inducibility of ventricular tachycardia is performed during ICD implantation, and various noninvasive risk markers are tested after randomization. Primary endpoint is total mortality, and secondary objectives are quality-of-life issues as well as cost-effectiveness ratio.

Adult↗
PubMed2003

Coronary surgery with non-cardioplegic methods in patients with advanced left ventricular dysfunction: immediate and long term results.

OBJECTIVE: To evaluate perioperative results and long term survival in patients with severe left ventricular (LV) dysfunction undergoing coronary artery bypass grafting (CABG) using non-cardioplegic methods. METHODS: From April 1990 through December 1999, 4100 consecutive patients underwent isolated CABG using hypothermic ventricular fibrillation. Of these, 141 (3.4%) had severe LV dysfunction (ejection fraction < 30%). Mean age was 58.3 (9.6) years. 64 patients (45.4%) were in Canadian Cardiovascular Society class III or IV and 16 (11.3%) were subjected to urgent or emergent surgery. A previous myocardial infarction was recorded in 127 (90.1%). The majority (89.4%) had triple vessel and 26 (18.4%) had left main disease. The mean number of grafts per patient was 3.1. At least one internal thoracic artery was used in all patients and 21 (14.8%) had bilateral internal thoracic artery grafts (1.2 arterial grafts per patient). RESULTS: Perioperative mortality was 2.8% (4 patients) and the incidence of acute myocardial infarction 2.8%. 50 (35.5%) patients required inotropes but only 16 (11.3%) required it for longer than 24 hours; 5 patients (3.5%) needed mechanical support. The incidence of renal failure was 3.5%. Mean duration of hospital stay was 9.6 (8.3) days. Follow up was 95% complete and extended for a mean of 57 (30) months. Late mortality was 11.5%. Actuarial survival rates at 1, 3, and 5 years were 96%, 91%, and 86%, respectively. CONCLUSIONS: Non-cardioplegic techniques are safe and effective in preserving the myocardium during CABG in patients with coronary artery disease and poor LV function, with low operative mortality and morbidity, and encouraging medium to long term survival rates.

Blood Vessel Prosthesis Implantation↗
PubMed2005

Isovolumic but not ejection phase Doppler tissue indices detect left ventricular dysfunction caused by coronary stenosis.

BACKGROUND: Isovolumic acceleration (IVA) obtained by tissue Doppler echocardiography (TDE) is a sensitive and relatively load-independent index for assessing systolic ventricular function. IVA also has the ability to describe the force-frequency relationship during incremental atrial pacing in vivo. OBJECTIVE: We sought to assess the ability of IVA to detect global left ventricular (LV) dysfunction induced by coronary constriction. METHODS: In 6 open-chest anesthetized pigs we examined right ventricular and LV long-axis function by TDE (4-chamber view) with simultaneous invasive measurements of intraventricular pressure, maximum dP/dt, minimum dP/dt, and tau by microtip catheter. A pneumatic cuff was placed around the proximal portion of left anterior descending coronary artery (LAD) and distal flow was monitored by transonic flow probe. Mean arterial pressures were monitored by indwelling cannula. Baseline studies assessed force-frequency relationships with TDE and invasive measurements during incremental pacing from 100 to 200/min (20/min increments every 10 minutes). The protocol was repeated 10 minutes after balloon inflation to reduce LAD blood flow by 50%. RESULTS: Compared with baseline, LV pressure decreased significantly (P = .03, 2-way analysis of variance) as did maximum dP/dt (P < .004) with LAD constriction. At the same time IVA and isovolumic velocity at the LV free wall were significantly reduced (P < .002 and P = .04, respectively) and both IVA and isovolumic velocity were correlated with dP/dt (r = 0.45, P < .002, and r = 0.35, P < .02, respectively). TDE systolic indices were unchanged in the right ventricle. CONCLUSION: IVA detects changes in global LV systolic function during LAD constriction and may be a useful clinical tool to diagnose ischemia.

Animals↗
PubMed1997

Angiotensin-converting enzyme inhibition and angiotensin II subtype-1 receptor blockade during the progression of left ventricular dysfunction: differential effects on myocyte contractile processes.

Inhibition of the angiotensin-converting enzyme (ACE) in the setting of chronic left ventricular (LV) dysfunction has been demonstrated to have beneficial effects on survival and symptoms. However, whether ACE inhibition has direct effects on myocyte contractile processes and if these effects are mediated primarily through the AT1 angiotensin-II receptor subtype remains unclear. The present project examined the relationship between changes in LV and myocyte function and beta adrenergic receptor transduction in four groups of six dogs each: (1) Rapid Pace: LV failure induced by chronic rapid pacing (4 weeks; 216 +/- 2 bpm); (2) Rapid Pace/ACEI: concomitant ACE inhibition (ACEI: fosinopril 30 mg/kg b.i.d.) with chronic pacing; (3) Rapid Pace/AT1 Block: concomitant AT1 Ang-II receptor blockade [Irbesartan: SR 47436(BMS-186295) 30 mg/kg b.i.d.] with chronic pacing; and (4) CONTROL: sham controls. With Rapid Pace, the LV end-diastolic volume increased by 62% and the ejection fraction decreased by 53% from control. With Rapid Pace/ACEI, the LV end-diastolic volume was reduced by 24% and the ejection fraction increased by 26% from Rapid Pace only values. Rapid Pace/AT1 Block did not improve LV geometry or function from Rapid Pace values. Myocyte contractile function decreased by 40% with Rapid Pace and increased from this value by 32% with Rapid Pace/ACEI. Rapid Pace/AT1 Block had no effect on myocyte function when compared with Rapid Pace values. With Rapid Pace/ACEI, beta receptor density and cyclic AMP production were normalized and associated with an improvement in myocyte beta adrenergic response compared with Rapid Pace only. Although Rapid Pace/AT1 also normalized beta receptor density, cyclic AMP production was unchanged and myocyte beta adrenergic response was reduced by 15% compared with Rapid Pace only. ACE inhibition with chronic rapid pacing improved LV and myocyte geometry and function, and normalized beta receptor density and cyclic AMP production. However, AT1 Ang-II receptor blockade with chronic rapid pacing failed to provide similar protective effects on LV and myocyte geometry and function. These unique findings suggest that the effects of ACE inhibition on LV geometry and myocyte contractile processes in the setting of developing LV failure are not primarily caused by modulation of AT1 Ang-II receptor activation.

Angiotensin Receptor Antagonists↗