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PubMed1994

Quality of life among 5,025 patients with left ventricular dysfunction randomized between placebo and enalapril: the Studies of Left Ventricular Dysfunction. The SOLVD Investigators.

OBJECTIVES: This study was performed to assess the quality of life of patients with left ventricular dysfunction for up to 2 years after randomization to enalapril or placebo. BACKGROUND: Previous reports have documented that survival of patients with congestive heart failure can be extended by the angiotensin-converting enzyme inhibitor enalapril. However, it is unknown whether enalapril has a long-term favorable impact on the quality of life in patients with heart failure. METHODS: A brief quality of life questionnaire assessing the quality of life was administered at baseline and at 6 weeks, 1 year and 2 years of follow-up to patients randomized to placebo or enalapril in the Studies of Left Ventricular Dysfunction (SOLVD). Participants had an ejection fraction < or = 0.35, no other serious illnesses and either symptomatic heart failure (treatment trial, n = 2,465) or asymptomatic left ventricular dysfunction (prevention trial, n = 2,560). RESULTS: Among the 14 scales of quality of life, better scores at one or more follow-up intervals were noted in 6 scales in the treatment trial and in 1 scale in the prevention trial among patients assigned to enalapril. Consistent superiority with enalapril at two consecutive follow-up intervals was noted in the treatment trial for social functioning and dyspnea but for no scale in the prevention trial. However, an average of 40% of quality of life responses were missing at 2 years of follow-up because of death or failure to complete the questionnaire. In the treatment trial, survivors with more severe heart failure were less likely to complete the questionnaire. CONCLUSIONS: Modest benefits in quality of life for > or = 1 year occurred when patients with left ventricular dysfunction and symptomatic heart failure were treated with enalapril. No apparent beneficial or adverse effect on quality of life was observed with enalapril in asymptomatic patients with left ventricular dysfunction.

Activities of Daily Living↗
PubMed1995

[Surgical results of aortic stenosis with or without left ventricular dysfunction--postoperative change of left ventricular function].

Between January 1980 and December 1992, 82 patients with aortic stenosis underwent isolated aortic valve replacement at our institution. Age of the patients ranged from 26 to 72 (58 +/- 6.4) years, and 58 were men and 24 were women. The patients were divided into two groups according to preoperative left ventricular ejection fraction (LVEF): 23 patients (LVEF < 50%, mean 39.7%; Group D) and 59 patients (LVEF > or = 50%, mean 62.6%; Group N). By means of echocardiography, LV function were evaluated before and at one month after operation in terms of left ventricular fractional shortening (LVFS), left ventricular systolic internal diameter (LVIDs), left ventricular mass index (LVMI), and left ventricular end systolic wall stress (ESWS). Postoperative early mortality including hospital death was 8.7% in group D (2 cases; myocardial infarction 1, cerebral complication 1) and 3.3% in group N (2 cases; myocardial infarction 1, low output syndrome 1), and this difference was not significant (NS) between two groups. The 5- and 12-year actuarial survival rate were 87.8% and 87.8% in group D, 91.5% and 87.6% in group N, respectively (NS). LVFS (pre/post) was 0.25 %/- 0/08/0.24 +/- 0.10 in group D, 0.38 +/- 0.10/0.32 +/- 0.10 in group N. The difference were significant before (p < 0.0005) and after (p < 0.005) operation between two groups. LVIDs (mm; pre/post) were 39.0 +/- 7.9/35.0 +/- 9.6 in group D, 28.7 +/- 7.3/229.3 +/- 7.6 in group N. The difference were significant before (p < 0.0005) and after (p < 0.01) operation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2006

Quantification of the risk and predictors of hyperkalemia in patients with left ventricular dysfunction: a retrospective analysis of the Studies of Left Ventricular Dysfunction (SOLVD) trials.

BACKGROUND: Limited data are available to predict the occurrence of hyperkalemia. Risk assessment is complicated by the lack of consistency of definition between trials. METHODS: We conducted a retrospective analysis of the SOLVD to evaluate the incidence of hyperkalemia and the value of several baseline characteristics as predictors of hyperkalemia in patients with left ventricular dysfunction. RESULTS: The incidence of hyperkalemia was 6.0% and 1.1% using a definition of > or = 5.5 and > or = 6.0 mmol/L, respectively. Independent predictors of hyperkalemia (> or = 5.5 mmol/L) were randomization to enalapril, baseline serum creatinine, serum potassium, New York Heart Association functional class III or IV, a history of diabetes, and atrial fibrillation (all P < .05). The use of loop diuretics was also associated with an increased risk of hyperkalemia but only in patients included in the SOLVD prevention trial. Similar results were obtained when renal function was evaluated using the estimated creatinine clearance. CONCLUSIONS: The definition of hyperkalemia is important when evaluating its incidence in clinical trials. Renal dysfunction, baseline serum potassium, diabetes, atrial fibrillation, New York Heart Association functional class, and treatment with an angiotensin-converting enzyme inhibitor are factors associated with the development of hyperkalemia in patients with left ventricular dysfunction. More specifically, our results suggests that before initiating drugs that can cause hyperkalemia in patients with heart failure, a strong consideration should be given to calculate creatinine clearance and that patients with a creatinine clearance < 60 mL/min should undergo a close monitoring of their serum potassium to prevent the development of hyperkalemia.

Aged↗
PubMed2000

Echocardiographic predictors of clinical outcome in patients with left ventricular dysfunction enrolled in the SOLVD registry and trials: significance of left ventricular hypertrophy. Studies of Left Ventricular Dysfunction.

OBJECTIVES: To assess the relation of left ventricular (LV) and left atrial (LA) dimensions, ejection fraction (EF) and LV mass to subsequent clinical outcome of patients with LV dysfunction enrolled in the Studies of Left Ventricular Dysfunction (SOLVD) Registry and Trials. BACKGROUND: Data are lacking on the relation of LV mass to prognosis in patients with LV dysfunction and on the interaction of LV mass with other measurements of LV size and function as they relate to clinical outcome. METHODS: A cohort of 1,172 patients enrolled in the SOLVD Trials (n = 577) and Registry (n = 595) had baseline echocardiographic measurements and follow-up for 1 year. RESULTS: After adjusting for age, New York Heart Association (NYHA) functional class, Trial vs. Registry and ischemic etiology, a 1-SD difference in EF was inversely associated with an increased risk of death (risk ratio, 1.62; p = 0.0008) and cardiovascular (CV) hospitalization (risk ratio, 1.59; p = 0.0001). Consequently, the other echo parameters were adjusted for EF in addition to age, NYHA functional class, Trial vs. Registry and ischemic etiology. A 1-SD difference in LV mass was associated with increased risk of death (risk ratio of 1.3, p = 0.012) and CV hospitalization (risk ratio of 1.17, p = 0.018). Similar results were observed with the LA dimension (mortality risk ratio, 1.32; p < 0.02; CV hospitalizations risk ratio, 1.18; p < 0.04). Likewise, LV mass > or =298 g and LA dimension > or =4.17 cm were associated with increased risk of death and CV hospitalization. An end-systolic dimension >5.0 cm was associated with increased mortality only. A protective effect of EF was noted in patients with LV mass > or =298 g (those in the group with EF >35% had lower mortality) but not in the group with LV mass <298 g. CONCLUSIONS: In patients with LV dysfunction enrolled in the SOLVD Registry and Trials, increasing levels of hypertrophy are associated with adverse events. A protective effect of EF was noted in patients with LV mass > or =298 g (those in the group with EF >35% fared better) but not in the group with LV mass <298 g. These data support the development and use of drugs that can inhibit hypertrophy or alter its characteristics.

Aged↗
PubMed1990

Ventricular arrhythmias in hypertensive left ventricular hypertrophy. Relationship to coronary artery disease, left ventricular dysfunction, and myocardial fibrosis.

Ventricular arrhythmias occur with increased frequency in hypertensive patients with left ventricular hypertrophy (LVH). The relationships, however, between ventricular arrhythmias and coexistent coronary artery disease, left ventricular dysfunction and left ventricular fibrosis have not been examined in hypertensive LVH. We carried out coronary arteriography on fifteen hypertensive patients with LVH and nonsustained ventricular tachycardia (greater than or equal to 3 consecutive ventricular complexes) of whom nine (60%) were free of significant (greater than 50% stenosis) coronary disease. To identify other possible correlates of left ventricular arrhythmias, 28 patients with LVH, comprising 17 with ventricular tachycardia and 11 without ventricular arrhythmias, underwent quantitative assessment of left ventricular function (angiographic ejection fraction), left ventricular mass (echocardiography), and left ventricular fibrosis (endomyocardial biopsy). Ejection fraction was not significantly different between the two groups (53 +/- 8% v 62 +/- 2%, P = NS). However, left ventricular mass was significantly greater (442 +/- 28 g v 339 +/- 34 g, P less than .05) and percentage fibrosis significantly higher (19 +/- 4% v 3 +/- 1%, P less than .001) in those patients with ventricular tachycardia. Thus ventricular arrhythmias in hypertensive patients with LVH cannot be entirely attributed to coexistent coronary disease, nor to left ventricular dysfunction, but are related to the degree of cardiac hypertrophy and subendocardial fibrosis.

Biopsy↗
PubMed2005

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

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

Aged↗
PubMed2001

Modified Glenn connection for acutely ischemic right ventricular failure reverses secondary left ventricular dysfunction.

BACKGROUND: Right heart failure after cardiopulmonary bypass can result in severe hemodynamic compromise with high mortality, but the underlying mechanisms remain poorly understood. After ischemia-induced right ventricular failure, alterations in the interventricular septal position decrease left ventricular compliance and limit filling but may also distort left ventricular geometry and compromise contractility and relaxation. This study investigated the effect of acute isolated right ventricular ischemia on biventricular performance and interaction and the response of subsequent right ventricular unloading by use of a modified Glenn shunt. METHODS: In 8 pigs isolated right ventricular ischemic failure was induced by means of selective coronary ligation. A modified Glenn circuit was then established by a superior vena cava-pulmonary artery connection. Ventricular performance was determined by conductance catheter-derived right ventricular pressure-volume loops and left ventricular pressure-segment length loops. Hemodynamic data at baseline, after right ventricular ischemia, and after institution of the Glenn circuit were obtained during inflow occlusion, and the load-independent contractile indices were derived. RESULTS: Right ventricular free-wall ischemia resulted in acute right ventricular dilation (118 +/- 81 mL vs 169 +/- 70 mL, P =.0008) and impairment of left ventricular contractility indicated by the reduced end-systolic pressure-volume relation slope (50.0 +/- 19 mm Hg/mm vs 18.9 +/- 8 mm Hg/mm, P =.002) and preload recruitable stroke work index slope (69.6 +/- 26 erg x cm(-3) x 10(3) vs 39.7 +/- 13 erg x cm(-3) x 10(3), P =.003). In addition, left ventricular relaxation (tau) was significantly prolonged (33.3 +/- 10 ms vs 53.0 +/- 16 ms, P =.012). Right ventricular unloading with the Glenn shunt reduced right ventricular dilation and significantly improved left ventricular contraction, end-systolic pressure-volume relation slope (18.9 +/- 8 mm Hg/mm vs 35.8 +/- 18 mm Hg/mm, P =.002), preload recruitable stroke work index slope (39.7 +/- 26 erg x cm(-3) x 10(3) vs 63.0 +/- 22 erg x cm(-3) x 10(3), P =.003), and diastolic performance (tau 53.0 +/- 16 ms vs 43.5 +/- 13 ms, P =.001). CONCLUSIONS: Right ventricular ischemia-induced dilation resulted in acute impairment of left ventricular contractility and relaxation. A modified Glenn shunt attenuated the left ventricular dysfunction by limiting right ventricular dilation and restoring left ventricular cavity geometry.

Animals↗
PubMed1990

Cardiac tamponade in left ventricular dysfunction.

Echocardiographic and hemodynamic data were measured in closed-chest dogs during graded cardiac tamponade (pericardial pressure 5, 10, and 15 mm Hg) before and after production of diffuse ischemic left ventricular dysfunction. Left ventricular dysfunction was produced by intracoronary injection of nonradioactive microspheres (54 +/- 3.9 mm diameter). Changes in left atrial pressure with cardiac tamponade were influenced by coexisting left ventricular dysfunction. Left atrial pressure increased with tamponade and was equal to pericardial pressure before left ventricular dysfunction was produced. However, after left ventricular dysfunction was produced, left atrial pressure was significantly higher than pericardial pressure before tamponade, but it fell toward pericardial pressure when tamponade was produced. Pulsus paradoxus (greater than 10 mm Hg) was present in all animals with cardiac tamponade before left ventricular dysfunction but in only one animal afterward. During each level of tamponade, the inspiratory fall of aortic systolic pressure was greater before than with left ventricular dysfunction. The slope of the linear regression between pericardial pressure and millimeters of mercury of inspiratory fall in aortic systolic pressure was significantly greater before than with left ventricular dysfunction (0.74 +/- 0.12 versus 0.32 +/- 0.12, p less than 0.05). Left ventricular dysfunction caused a leftward and upward shift of the pericardial pressure-volume relation. As a result, right atrial and ventricular collapse occurred with significantly smaller volumes of pericardial fluid after than before left ventricular dysfunction. We conclude that pulsus paradoxus may be absent in cardiac tamponade with coexisting left ventricular dysfunction and unequal filling pressures. Echocardiographic signs of cardiac tamponade may occur with small effusions in the presence of left ventricular dysfunction.

Animals↗
PubMedDate not supplied

Cold infarction areas of varying size in the presence of left ventricular dysfunction: the impact on left ventricular ejection fraction determination by gated SPECT compared to radionuclide ventriculography.

The agreement in left ventricular (LV) ejection fraction (EF) determination between the gated perfusion SPECT (GPS) and radionuclide ventriculography (RVG) methods has been reported to show a systematic reduction with increasing EF values. In some reports, this EF difference exceeds 5%, indicating a critical underestimation rate by GPS in terms of clinical reliability. Although the accuracy of endocardial edge detection by means of GPS proves to be reliable, even in patients with large perfusion defects, the accuracy of EF calculation seems to depend on the level of individual EF values. Our objective was to investigate the RVG-GPS agreement in EF determination specifically in patients with myocardial infarction (MI) having perfusion defects including extremely depleted areas and LV dysfunction. Our patients had a EF<50%, a population in which the best agreement values between the above two methods should be found according to the literature. The idea was to test the accuracy of QGS algorithm in the presence of cold perfusion defects and a low probability of EF level influence. Thirty-six patients (26 males; 61.8+/-9.1 y and 10 female; 64.1+/-10.7 y) with MI older than two weeks, having perfusion defects, including all regions of varying size with no visible tracer uptake in rest GPS and RVG-EF<50% were included in the study. Rest-GPS was performed by injecting iv 925 MBq 99mTc-sestamibi (8-time bins) using a dual-headed gamma camera and rest-RVG was performed within the following three days by injecting iv 740 MBq 99mTc-pertechnetate-pyrophosphate (24 time bins). Myocardial perfusion was visually analyzed on a 17 segment-model and summed rest perfusion scores (SRS) were determined. The cold defect number (CDN) was calculated by selecting the myocardial segments with 0%-9% of maximal tracer uptake (grade 4) to identify the extent of the depleted tissue in each patient. The patients with (3)4 adjacent myocardial segments with grade 4 perfusion were considered as having large cold defects (Group 1: GR1). Patients with two or three CDN constituted the Group 2 (GR2; medium cold defects) and those with only one CDN constituted Group 3 (GR3; small cold defects). Hereafter, the relative weight of cold perfusion defects (CD%) and infarcted segments (IS%) were calculated for all patients and subgroups. Of 36 patients studied, 14 patients (39%, GR1) had large cold defects. Eleven patients (30.5%, GR2) had moderate and 11 (30.5%, GR3) had small cold defects. The overall mean value of CDN was 3.03+/-1.96 (1-9). Mean EF values in RVG and GPS among Groups 1, 2 and 3 were 28.78%+/-6.32%, 38.46%+/-6.43%, 38.73%+/-8.55% and 27.0%+/-6.93%, 37.82%+/-8.80%, 33.27%+/-11.65%, respectively. The percentage of patients showing an EF difference pound 5% between RVG and GPS in Groups 1, 2 and 3 were 93%, 73% and 27%, respectively. The CD% and IS% were 19+/-12, 30+/-7, 14+/-3, 6 and 52+/-20, 61+/-18, 50+/-17, 42+/-23 in overall, GR1, GR2 and GR3, respectively. It is concluded that: the negligible underestimation of EF in GR1 by GPS compared to RVG confirms the stability of the geometric modeling algorithm of QGS in this particular patient sub-group. Although the agreement results in patients with smaller defects were probably influenced through the realization of RVG and GPS studies performed on different days, it seems to be rational to set the threshold of RVG-GPS agreement dependency on EF levels in patients with myocardial infarction lower than 50%.

Female↗
PubMed2001

Coronary artery bypass grafting in patients with severe left ventricular dysfunction: predictive significance of left ventricular diastolic filling pattern.

AIMS: The aim of our study was to evaluate the influence of left ventricular (LV) diastolic filling impairment on postoperative results in patients (pts) with low LV ejection fraction (EF) (<35%) undergoing coronary artery bypass grafting (CABG). METHODS: The study covered 56 patients (mean age 58.9 +/- 17.1 years). Two dimensional Doppler echocardiographic investigations were performed pre- and 10-14 days post-CABG. Patients were divided into three groups according to the LV diastolic filling. RESULTS: Early postoperative mortality rate (including perioperative period and 2 weeks after surgery) was highest in the restriction group (33%) vs. pseudonormalization (12.5%) vs. impaired relaxation (13.6%). Postoperative cardiovascular complications rate was highest also in the restriction group, 55.5%, and did not differ between pseudonormalization (25%) and impaired relaxation group (27.2%). Logistic regression analysis showed that restrictive LV filling pattern, early diastolic filling deceleration time and LV end-diastolic diameter independently influence perioperative mortality. In the early postoperative period mean LV wall motion score (WMS) did not improve in 8/19 (42%), 6/14 (43%) and 8/12 (67%) patients, respectively, in the impaired relaxation, pseudonormalization and restriction group. CONCLUSIONS: In patients with severe LV dysfunction undergoing CABG, impaired relaxation and pseudonormal pattern of LV diastolic filling correlated with postoperative improvement in LV regional contraction, while restrictive pattern correlated with high early postoperative mortality, morbidity and minimal improvement in LV systolic function. Restrictive LV filling pattern, early diastolic filling deceleration time and LV end-diastolic diameter were found to be independent predictors of perioperative mortality.

Adult↗
PubMed1994

Tolerability of enalapril initiation by patients with left ventricular dysfunction: results of the medication challenge phase of the Studies of Left Ventricular Dysfunction.

Although converting-enzyme inhibitors are useful for the treatment of congestive heart failure (CHF), there are concerns about adverse reactions especially on initiation of therapy. In the Studies of Left Ventricular Dysfunction, enalapril, 2.5 mg twice per day was given on an open-label outpatient basis for 7 days (mean 6.1, range 2 to 7, and median 7) as a prerandomization drug challenge to 7487 patients with left ventricular dysfunction (ejection fraction < or = 0.35). Four hundred forty-four (5.93%) patients reported side effects, including symptoms attributed to hypotension (in 166 patients [2.2%]). The majority (346 [77.9%] of 444 and 129 [77.7%] of 166 with symptoms attributed to hypotension) of patients who reported side effects were willing to participate in the study and to continue receiving enalapril. Thus only 98 (1.3%) of 7487 patients (0.5% because of symptoms attributed to hypotension) were not willing to continue because of side effects. Women and patients of CHF class III or IV were more likely to report side effects. In conclusion, enalapril is well tolerated by patients with left ventricular dysfunction; treatment can be initiated on an outpatient basis in the majority of patients.

Enalapril↗
PubMed1990

Comparison of neuroendocrine activation in patients with left ventricular dysfunction with and without congestive heart failure. A substudy of the Studies of Left Ventricular Dysfunction (SOLVD).

Neuroendocrine activation is known to occur in patients with congestive heart failure, but there is uncertainty as to whether this occurs before or after the presence of overt symptoms. In the Studies of Left Ventricular Dysfunction (SOLVD), a multicenter study of patients with ejection fractions of 35% or less, we compared baseline plasma norepinephrine, plasma renin activity, plasma atrial natriuretic factor, and plasma arginine vasopressin in 56 control subjects, 151 patients with left ventricular dysfunction (no overt heart failure), and 81 patients with overt heart failure before randomization. Median values for plasma norepinephrine (p = 0.0001), plasma atrial natriuretic factor (p less than 0.0001), plasma arginine vasopressin (p = 0.006), and plasma renin activity (p = 0.03) were significantly higher in patients with left ventricular dysfunction than in normal control subjects. Neuroendocrine values were highest in patients with overt heart failure. Plasma renin activity was normal in patients with left ventricular dysfunction without heart failure who were not receiving diuretics and was significantly increased (p less than 0.05) in patients on diuretic therapy. We conclude that neuroendocrine activation occurs in patients with left ventricular dysfunction and no heart failure. Neuroendocrine activation is further increased as overt heart failure ensues and diuretics are added to therapy.

Arginine Vasopressin↗
PubMed2004

Effects of diabetes mellitus and ischemic heart disease on the progression from asymptomatic left ventricular dysfunction to symptomatic heart failure: a retrospective analysis from the Studies of Left Ventricular Dysfunction (SOLVD) Prevention trial.

BACKGROUND: Emerging data suggest that diabetes mellitus is a risk factor for the progression of established heart failure only in those patients with ischemic cardiomyopathy. Whether diabetes mellitus is a risk factor for the progression from asymptomatic left ventricular systolic dysfunction to symptomatic heart failure in patients with left ventricular dysfunction of an ischemic cause is not known. METHODS: We performed a retrospective analysis of 2821 patients with asymptomatic left ventricular systolic dysfunction from the Studies of Left Ventricular Dysfunction (SOLVD) Prevention trial. We used adjusted survival analysis to examine the effects of ischemic heart disease and diabetes mellitus on 3 prespecified study end points: (1) development of heart failure (HF) symptoms, (2) HF hospitalization, and (3) death or development of symptoms. RESULTS: There is a statistically significant interaction between the cause of left ventricular systolic dysfunction and diabetes mellitus on the risk of development of heart failure symptoms (P = .020). Patients with ischemic cardiomyopathy and diabetes had an increased risk of progression to symptomatic heart failure (HR = 1.56, P < .001), hospitalization for heart failure (HR = 2.16, P < .001), and death or development of symptoms (HR = 1.50, P < .001), compared with patients with ischemic cardiomyopathy without diabetes. In contrast, diabetes was not associated with an increased risk of reaching these end points in patients with nonischemic cardiomyopathy. CONCLUSIONS: Diabetes mellitus is a risk factor for the progression from asymptomatic left ventricular systolic dysfunction to symptomatic heart failure, but this risk appears to be confined to those patients with ischemic cardiomyopathy.

Analysis of Variance↗
PubMed1987

Antiarrhythmic efficacy and hemodynamic effects of cibenzoline in patients with nonsustained ventricular tachycardia and left ventricular dysfunction.

This was a prospective single-blind, placebo-controlled study of cibenzoline in 21 patients with five or more runs of nonsustained ventricular tachycardia (VT) and left ventricular dysfunction (mean left ventricular ejection fraction 36 +/- 24%). Ambulatory electrocardiographic monitoring revealed a baseline of 616 +/- 431 runs of VT/day on placebo. Of the 18 patients tolerating the drug, 14 (77%) patients initially had a 75% or greater reduction in VT (177 +/- 164 runs of VT/day, p less than .05). A repeat ambulatory electrocardiogram documented long-term suppression of VT in 13 of 14 patients at 1 month (2.1 +/- 1.3 runs VT/day, p less than .01), in 10 of 14 patients at 3 months (2.5 +/- 1.9 runs VT/day, p less than .01), and in nine of 14 patients at 6 months (1.5 +/- 0.8 runs VT/day, p less than .01). Aggravation of arrhythmia or drug failure was seen in four of 18 (22%) patients (new onset of sudden cardiac death, two patients; sustained VT, two patients). Hemodynamic measurements were obtained with the use of right heart catheterization in patients at rest and exercising during the placebo phase and after 60 hr of oral cibenzoline. Group hemodynamic variables, both measured and derived, showed no detrimental effect of cibenzoline. However, in three of 21 patients (mean ejection fraction 21%), cibenzoline was discontinued due to severe depression of left ventricular function. Caution is recommended in the use of cibenzoline in patients with left ventricular ejection fractions of less than 25%.

Aged↗
PubMed2005

Surgical ventricular remodeling for patients with clinically advanced congestive heart failure and severe left ventricular dysfunction.

BACKGROUND: Surgical ventricular remodeling (SVR) is an accepted therapy for post-infarction ventricular remodeling. Current literature on SVR outcomes has focused on heterogeneous populations with regard to left ventricular function and New York Heart Association (NYHA) class. We assessed outcomes after SVR in patients with advanced congestive heart failure (CHF) (NYHA Class III/IV) and a pre-operative ejection fraction (EF) < or =20%. METHODS: Data were analyzed for 51 consecutive SVR patients from January 2002 to June 2004. Cardiac catheterization, echocardiography and magnetic resonance imaging (MRI) identified 62.7% (32 of 51) of patients with an EF < or =20%, with the majority having an EF < or =15% (65.6%; 21 of 32). Cox regression analysis was performed to determine predictors of mortality in patients with an EF < or =20%. Follow-up was 100% (32 of 32) complete. RESULTS: Mean age was 61.9 +/- 10.3 (range 40 to 80) years with a male:female ratio of 27:5. Operative mortality was 6.3% (2 of 32). Twenty-two percent (7 of 32) had concomitant mitral valve procedures. Follow-up demonstrated a statistically significant improvement in left ventricular volumes and EF in survivors. Cox regression analysis identified the following to be significant predictors of mortality: pre-operative left ventricular end-systolic volume index >130 ml/m2; pre-operative diabetes; and intra-aortic balloon pump usage. Pre-operatively, all patients (32 of 32) were categorized as NYHA Class III/IV, with 69% (22 of 32) improving to NYHA Class I/II at follow-up (p < 0.01). Survival did not differ statistically between patients with an EF < or =20% and an EF >20% (n = 19). CONCLUSIONS: Our results indicate that SVR improves left ventricular function and functional status for patients with advanced CHF and a pre-operative EF < or =20%. Therefore, SVR is a viable surgical alternative for patients with severe left ventricular dysfunction.

Aged↗
PubMed2003

Non-transplant surgery for heart failure and severe left ventricular dysfunction. Opportunities and limitations.

The need of alternatives to transplantation has lead to routinely reconsidering conventional surgery for selected patients with advanced heart failure. Although the recovery of ventricular contractility with revascularization sometimes restores ventricular function almost to normality while dramatically enhancing the quality of life, only a few patients with ischemic left ventricular dysfunction exhibit the amount of hibernating myocardium required for such a spectacular outcome taking place. Advanced remodeling is a further obstacle and is currently being addressed by means of operations designed to reduce ventricular volume and restore geometry. Hemodynamic measurements raise concerns, however, as to the diastolic function and the competence of the mitral valve late after reconstructive surgery. Finally, the repair of mitral valve regurgitation has produced interesting short-to-medium term results both in terms of survival and heart failure relief. Yet, their durability is uncertain, if not disappointing when the valvular disease has an ischemic etiology. Expectations of patients undergoing one of the aforementioned procedures, or a combination thereof, should not be averaged as they heavily depend on the specific patient profile under evaluation.

Cardiac Surgical Procedures↗
PubMed2003

Aortic valve replacement in severe aortic stenosis with left ventricular dysfunction: determinants of cardiac mortality and ventricular function recovery.

OBJECTIVE: The influence of left ventricular (LV) dysfunction on survival of patients with severe aortic stenosis is poorly characterized. Few data are available about preoperative predictors of cardiac mortality and LV function recovery after aortic valve replacement of such patients. The aim of our study was to examine the outcome and the preoperative predictors of postoperative cardiac death and of LV function recovery in these patients. METHODS: We evaluated 85 consecutive patients with severe aortic stenosis (aortic valve area <1 cm(2)) and severe depression of LV ejection fraction (EF) <35% at cardiac catheterization. Among them, 52 underwent aortic valve replacement and they were compared to patients who were not operated on. All patients had a mean clinical follow-up of 53 months and 94% of them had a mean echocardiographic follow-up of 14 months after aortic valve replacement. RESULTS: The mean baseline characteristics included: LVEF 28+/-6%, peak-to-peak transvalvular gradient 51+/-29 mmHg, aortic valve area 0.63+/-0.25 cm(2). Thirty-three patients did not undergo aortic valve replacement: 32 of them died within 3 years. Fifty-two patients underwent aortic valve replacement and 16 had a concomitant coronary bypass surgery. In-hospital mortality was 8%. Postoperative NYHA functional class changed from 2.84+/-0.67 to 1.43+/-0.44 (P<0.001) and LVEF from 29+/-6% to 43+/-10% (P<0.001). At follow-up 10 patients died of heart disease. By multivariate analysis, preoperative LV end-systolic volume index (ESVI) was the only covariate of cardiac death (LVESVI/10 ml/m(2), OR 1.3, CI 1.1-1.8, P<0.028). By using a receiver operating characteristic curve, LVESVI< or =90 ml/m(2) was the best cut-off value (sensitivity and specificity 78%) to fit with a better survival (93% vs. 63%, P<0.01) and with LVEF recovery after aortic valve replacement (EF improved by 15+/-10% vs. 8+/-5%, P<0.001). CONCLUSIONS: Despite LV dysfunction, aortic valve replacement appears to change drastically the natural history of severe aortic stenosis. Preoperative LV levels predict different postoperative survival rate and LVEF recovery.

Adult↗