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PubMed1997

How European cardiologists perceive the role of calcium antagonists in the treatment of heart failure and left ventricular dysfunction.

In a poll of European cardiologists, one of the most popular of the given definitions of heart failure centres on the abnormality of ventricular function. However, opinion remains divided on the necessity of a distinction between diastolic and systolic heart failure, as it does on the value and procedures of stress testing. The 'no-reflow' phenomenon continues to pose a challenge in conditions requiring myocardial reperfusion, and precise identification of some heart disorders apparently remains difficult in many cases. Drug treatment of conditions like left ventricular dysfunction of arterial hypertension is open to continuing discussion, but calcium antagonists seem assured of an important role.

Calcium Channel Blockers↗
PubMed2001

Effect of carvedilol on outcome after myocardial infarction in patients with left-ventricular dysfunction: the CAPRICORN randomised trial.

BACKGROUND: The beneficial effects of beta-blockers on long-term outcome after acute myocardial infarction were shown before the introduction of thrombolysis and angiotensin-converting-enzyme (ACE) inhibitors. Generally, the patients recruited to these trials were at low risk: few had heart failure, and none had measurements of left-ventricular function taken. We investigated the long-term efficacy of carvedilol on morbidity and mortality in patients with left-ventricular dysfunction after acute myocardial infarction treated according to current evidence-based practice. METHODS: In a multicentre, randomised, placebo-controlled trial, 1959 patients with a proven acute myocardial infarction and a left-ventricular ejection fraction of </=40% were randomly assigned 6.25 mg carvedilol (n=975) or placebo (n=984). Study medication was progressively increased to a maximum of 25 mg twice daily during the next 4-6 weeks, and patients were followed up until the requisite number of primary endpoints had occurred. The primary endpoint was all-cause mortality or hospital admission for cardiovascular problems. Analysis was by intention to treat. FINDINGS: Although there was no difference between the carvedilol and placebo groups in the number of patients with the primary endpoint (340 [35%] vs 367 [37%], hazard ratio 0.92 [95% CI 0.80-1.07]), all-cause mortality alone was lower in the carvedilol group than in the placebo group (116 [12%] vs 151 [15%], 0.77 [0.60-0.98], p=0.03). Cardiovascular mortality, non-fatal myocardial infarctions, and all-cause mortality or non-fatal myocardial infarction were also lower on carvedilol than on placebo. INTERPRETATION: In patients treated long-term after an acute myocardial infarction complicated by left-ventricular systolic dysfunction, carvedilol reduced the frequency of all-cause and cardiovascular mortality, and recurrent, non-fatal myocardial infarctions. These beneficial effects are additional to those of evidence-based treatments for acute myocardial infarction including ACE inhibitors.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Predicting postinfarction left ventricular dysfunction based on the configuration of the QRS complex and ST segment in the initial ECG of patients with a first anterior wall myocardial infarction.

The objective of the study was to identify patients with anterior wall acute myocardial infarction (AMI) at high risk of postinfarction left ventricular dysfunction (LVD). This study population included all patients admitted with a diagnosis of anterior wall AMI (ST segment elevation of > 1 mm in 2 or more precordial leads) without history or ECG evidence of antecedent AMI,who underwent assessment of left ventricular ejection fraction (LVEF) during emergency hospitalization. ST segment deviation from baseline was measured manually 0.08 s after the J point in all leads. Patients (n = 81) were classified into two groups based on the configuration of the QRS complex and ST segment: ST > 1 mm with preserved (pattern A; n = 60) or distorted terminal QRS (emergence of the J point at a level above the lower half of the R wave or disappearance of the S wave in leads with an Rs configuration; pattern B; n = 21). LVD (LVEF < 40%) was significantly more prevalent in patients with pattern B than pattern A (48 vs. 12%; p = 0.002). There was no correlation between the number of leads with ST segment elevation and LVD (p = 0.47). The sum of ST segment elevation in involved leads correlated weakly, yet significantly with LVEF (R = -0.22; p < 0.05). In conclusion, patients with anterior wall AMI and pattern B in the initial ECG are at high risk of post-AMILVD.

Adult↗
PubMed2000

Effects of long-term therapy with bosentan on the progression of left ventricular dysfunction and remodeling in dogs with heart failure.

OBJECTIVES: In this study, we examined the effects of long-term therapy with bosentan on the progression of LV dysfunction and remodeling in dogs with moderate HF. BACKGROUND: Acute intravenous administration of bosentan, a mixed endothelin-1 type A and type B receptor antagonist, was shown to improve left ventricular (LV) function in patients and dogs with heart failure (HF). METHODS: Left ventricular dysfunction was induced by multiple, sequential intracoronary microembolizations in 14 dogs. Embolizations were discontinued when LV ejection fraction (EF) was between 30% and 40%. Dogs were randomized to three months of therapy with bosentan (30 mg/kg twice daily, n = 7) or no therapy at all (control, n = 7). RESULTS: In untreated dogs, EF decreased from 35 +/- 1% before initiating therapy to 29 +/- 1% at the end of three months of therapy (p = 0.001), and LV end-diastolic volume (EDV) and end-systolic volume (ESV) increased (EDV: 71 +/- 3 vs. 84 +/- 8 ml, p = 0.08; ESV: 46 +/- 2 vs. 60 +/- 6 ml, p = 0.03). By contrast, in dogs treated with bosentan, EF tended to increase from 34 +/- 2% before initiating therapy to 39 +/- 1% at the end of three months of therapy (p = 0.06), and EDV and ESV decreased (EDV: 75 +/- 3 vs. 71 +/- 4 ml, p = 0.05; ESV: 48 +/- 2 vs. 43 +/- 3 ml, p = 0.01). Furthermore, compared with untreated dogs, dogs treated with bosentan showed significantly less LV cardiomyocyte hypertrophy and LV volume fraction of interstitial fibrosis. CONCLUSIONS: In dogs with moderate HF, long-term therapy with bosentan prevents the progression of LV dysfunction and attenuates LV chamber remodeling. The findings support the use of mixed endothelin-1 receptor antagonists as adjuncts to the long-term treatment of HF.

Animals↗
PubMed2004

Echocardiographic tamponade in severe left ventricular dysfunction: the impact of small pericardial effusion and the absence of pulsus paradoxicus.

Cardiac tamponade is a commonly encountered clinical entity. It is a clinical syndrome characterized by elevated filling pressures, pulsus paradoxicus, and eventually, hypotension. It occurs as intrapericardial pressure exceeds intracardiac pressures altering ventricular filling. Generally tamponade occurs with moderate or large accumulations of pericardial fluid that result in an increase in pericardial pressure. It is well known that rapid accumulation of relatively small volumes of fluid can cause tamponade pathophysiology. We report a less well-recognized phenomenon. In the setting of severe left ventricular dysfunction, small volumes of pericardial fluid can result in excessive intrapericardial pressure and echocardiographic tamponade in the absence of a significant pulsus paradoxicus.

Adult↗
PubMed1995

Costs and effects of enalapril therapy in patients with symptomatic heart failure: an economic analysis of the Studies of Left Ventricular Dysfunction (SOLVD) Treatment Trial.

The clinical results of the Studies of Left Ventricular Dysfunction (SOLVD) Treatment Trial have been published previously, but no evaluation of cost-effectiveness based on the primary data has been reported. The authors used a decision analytic model based on primary data from SOLVD to estimate years of survival (overall, by New York Heart Association Class, and quality-adjusted) and to estimate costs of nonfatal hospitalizations, ambulatory care, therapy with enalapril, and deaths. Clinical and resource utilization data were derived from participants in SOLVD, and cost data were derived from the United States. Therapy with enalapril during the approximate 48-month follow-up period in SOLVD resulted in a gain of 0.16 year of life and savings of dollars 718. During the patient's lifetime, a survival benefit of 0.40 year, a cost per year of life saved of dollars 80, and a cost per quality-adjusted life year of dollars 115 with the use of enalapril were projected. The results indicated a net savings and gain in life expectancy during the SOLVD treatment trial. The lifetime projection suggests that therapy with angiotensin-converting enzyme inhibitors, such as enalapril, is extremely attractive when compared with many commonly used interventions in patients with cardiovascular disease or heart failure.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2002

Assessment of sarcoplasmic reticulum Ca(2+) flux pathways in cardiomyocytes from rabbits with infarct-induced left-ventricular dysfunction.

The aim of the study was to correlate intracellular Ca(2+) transients with Ca(2+) uptake and efflux characteristics of the sarcoplasmic reticulum (SR) in ventricular myocytes isolated from rabbits with left-ventricular dysfunction (LVD). Chronic (8 weeks) ligation of a coronary artery caused marked LVD in rabbits. Measurements of intracellular [Ca(2+)] were made using Fura-2 on intact, single, left-ventricular myocytes. SR Ca(2+) flux rates associated with sarco-endoplasmic reticulum Ca(2+) ATPase type 2 (SERCA2)-mediated uptake, ryanodine receptor type 2 (RyR2)-mediated Ca(2+) efflux and background SR Ca(2+) leak were measured in suspensions of permeabilised myocytes. Measurements on single, permeabilised myocytes were used to assess the steady-state Ca(2+) content of the SR and the characteristics of spontaneous SR Ca(2+) release. Peak systolic [Ca(2+)] was significantly lower; time-to-peak and Ca(2+) transient duration were significantly longer in LVD myocytes. SERCA2-mediated Ca(2+) uptake was reduced to approximately 50% in myocytes from the LVD group. Ruthenium red (RuR)-sensitive Ca(2+) efflux (mediated by the RyR2) was also reduced in the LVD group by approximately 50%, as was the remaining (RuR-insensitive) background Ca(2+) leak. Measurements from single, permeabilised myocytes showed a lower steady-state SR Ca(2+) content. The frequency and amplitude of spontaneous SR Ca(2+) release from LVD hearts was also reduced. Partial inhibition of SERCA2 by thapsigargin depressed both the amplitude and the frequency of spontaneous release. Partial inhibition of RyR2-mediated-Ca(2+) efflux with tetracaine enhanced spontaneous Ca(2+) release amplitude and decreased frequency. Increased background Ca(2+) leak with ionomycin decreased the frequency of spontaneous release. It is concluded that partial inhibition of SERCA2 mimics some aspects of altered SR function in LVD, but reduced RyR2 function cannot explain the other functional alterations observed. Reduced background Ca(2+) leak from the SR may compensate partly for the reduced Ca(2+) uptake capacity of the SR in the LVD group.

Animals↗
PubMed1999

Dobutamine-atropine stress echocardiography for risk stratification in patients with chronic left ventricular dysfunction.

OBJECTIVE: To assess the prognostic value of sustained improvement, scar and inducible ischemia with or without viability in patients with chronic left ventricular dysfunction (LVD). BACKGROUND: Dobutamine-atropine stress echocardiography (DASE) accurately detects scar, reversible dysfunction and the extent of coronary artery disease in LVD. METHODS: Three hundred fifty consecutive patients (age 62+/-13 years, mean+/-SD, 215 men/135 women) with moderate to severe LVD (LVEF < 40%, mean 30+/-8%) underwent DASE and were followed for > or =18 months. Dobutamine-atropine stress echocardiographic findings were classified according to sustained improvement in all vascular territories, scar, inducible ischemia (worsening wall motion at peak dose only or biphasic responses) and their extent. RESULTS: Sustained improvement occurred in 83 patients (24%), scar alone in 99 (28%) and inducible ischemia in 168 (48%, with biphasic responses in 104). Ischemia was induced in all vascular territories in 26 patients. Patients with sustained improvement or scar alone were treated medically, whereas 46% (78/168) with inducible ischemia were revascularized (coronary bypass surgery, n = 67 or angioplasty, n = 11). There were 76 hard events including cardiac death in 59, nonfatal myocardial infarction in 11, and resuscitated sudden death in 6. Hard events were rare in sustained improvement (5%, 4/83), uncommon in scar (13%, 13/99) and common (p < 0.01) in medically treated patients with inducible ischemia (59%, 53/90). Cardiac deaths were especially common (p < 0.01) in patients with biphasic responses (55%, 28/51). Inducible ischemia independently predicted hard events (chi2 = 75.35, p < 0.001) along with reduced LVEF at peak dose (chi2 = 8.38, p = 0.004). Hard cardiac events were uncommon (8%, 6/78, p < 0.001) in patients with inducible ischemia who underwent early revascularization. CONCLUSIONS: Inducible ischemia during DASE was the major determinant of outcome in LVD and independent of clinical data and left ventricular function. Improved wall thickening alone and scar alone predicted good outcome. Survival of patients with inducible ischemia was better after revascularization.

Adult↗
PubMedDate not supplied

Role of helical CT in detecting right ventricular dysfunction secondary to acute pulmonary embolism.

OBJECTIVE: The purpose of this study was to evaluate the role of helical CT in detecting right ventricular dysfunction (RVD) after acute pulmonary embolism (PE). METHODS: This was a retrospective study consisting of 25 patients with CT scans positive for acute pulmonary embolism who had either follow-up echocardiography (23 patients) or pulmonary angiography (2 patients). CT scans were reviewed for findings suggestive of RVD. Scans were considered positive for RVD if the right ventricle (RV) was dilated or if the interventricular septum was deviated towards the left ventricle. Results were then correlated with the results of echocardiography or pulmonary angiography to estimate the sensitivity and specificity of CT in detecting RVD associated with PE. RESULTS: Within this group of 25 patients with PE, CT demonstrated sensitivity of 78% (7/9), specificity of 100% (16/16), and positive predictive value of 100% (7/7) in detection of RVD. CONCLUSION: CT may be useful in detecting RVD in patients with acute PE.

Acute Disease↗
PubMed2000

Augmented response in plasma brain natriuretic peptide to dynamic exercise in patients with left ventricular dysfunction and congestive heart failure.

OBJECTIVES: We have previously demonstrated that patients with symptomatic congestive heart failure (CHF), but not with asymptomatic left ventricular dysfunction (LVD), have augmented plasma atrial natriuretic peptide (ANP) response to exercise. Plasma brain natriuretic peptide (BNP) response to exercise is less extensively studied. The aim of this study was to determine whether responses of plasma BNP during exercise normalized for exercise workload are altered in patients with LVD and CHF. SUBJECTS AND METHODS: Twenty-nine patients with LVD, 32 patients with CHF (NYHA classes II-III) and 27 age-matched control subjects were studied. Ventilatory, plasma ANP and BNP responses were assessed during symptom-limited cardiopulmonary exercise testing. Plasma natriuretic peptide levels were measured at rest and immediately after peak exercise. The increment in plasma BNP was divided by the increment in oxygen uptake (VO2) from rest to peak exercise, and this ratio [BNP exercise ratio: (peak BNP - rest BNP)/(peak VO2 - rest VO2)] was compared amongst the three groups. RESULTS: Peak VO2 (Control, LVD and CHF: 28.2 +/- 1.7, 21.1 +/- 1.8, 16.2 +/- 0.6 ml, min(-1) kg(-1), respectively), anaerobic threshold and peak workload became smaller as heart failure worsened. Resting and peak plasma ANP levels were significantly higher only in CHF, whilst resting and peak plasma BNP levels displayed a significant and continuous increase from normal subjects to LVD and CHF. The ANP exercise ratio (1.25 +/- 0.36, 2.61 +/- 0.57, 7.72 +/- 1.65, ANOVA P = 0.0002) was significantly higher only in patients with CHF, whilst the BNP exercise ratio (0.35 +/- 0.10, 2.60 +/- 0.69, 4.98 +/- 0.97, ANOVA P = 0.0001) was significantly higher in patients with LVD and became progressively higher in patients with CHF. CONCLUSIONS: These data showed that the BNP exercise ratio, an exercise plasma BNP response normalized with exercise workload, was augmented in patients with LVD, and became progressively higher in CHF, suggesting that an augmented exercise BNP ratio exists early in the course of developing CHF.

Anaerobic Threshold↗
PubMed2004

Early and midterm outcome after off-pump coronary artery bypass grafting in patients with left ventricular dysfunction.

BACKGROUND: The purpose of this study was to define the early outcome and the potential for midterm survival in patients with left ventricular dysfunction (LVD) who undergo off-pump coronary artery bypass (OPCAB) and to compare these results with those of conventional coronary artery bypass grafting (CABG). METHODS: Medical records of patients with LVD (n = 732) between January 1998 and March 2002 were retrospectively reviewed. There were 523 patients with moderate LVD (ejection fraction, 30%-50%; 463 CABG versus 60 OPCAB) and 209 patients with severe LVD (ejection fraction, < 30%; 136 CABG versus 73 OPCAB). Midterm survival data (mean follow-up, 2.3 years) were obtained from the National Death Index. Groups were compared by multivariate Cox proportional hazard models, and Kaplan-Meier curves were plotted. RESULTS: CABG patients had lower European System for Cardiac Operative Risk Evaluation values (5.3 versus 7.2 and 8.0 versus 9.6 in moderate and severe LVD subgroups, respectively; P < .001). There were no differences (OPCAB versus CABG) in 30-day mortality (3.3% versus 1.9%, moderate LVD group, P = .366; 6.8% versus 4.4%, severe LVD group, P = .521), length of stay (9.3 versus 8.6 days, moderate LVD group, P = .683; 11.9 versus 11.8 days, severe LVD group, P = .423), and postoperative complications (13.3% versus 11.0%, moderate LVD group, P = 0.663; 16.4% versus 20.6%, severe LVD group, P = .581). Successful coronary bypass in patients with severe LVD was associated with 68.2% and 66.2% actuarial 48-month survival rates for the CABG and OPCAB patients, respectively (P = .336), and these rates rose to 86.0% and 82.9% in patients with moderate LVD (P = .121). When CABG patients with moderate LVD were considered the reference group, the adjusted hazard ratio of OPCAB patients with moderate LVD for midterm mortality was 1.32 (95% confidence interval, 0.61-2.87; P = .481). CABG and OPCAB patients with severe LVD had the same adjusted hazard ratio of 1.86, and this figure was statistically significant compared with the value for the reference group (P = .011 and P = .039, respectively). CONCLUSIONS: Patients with LVD can derive midterm benefit from coronary bypass. OPCAB in higher-risk patients had early and midterm outcomes similar to those of CABG.

Aged↗
PubMed1998

Influence of the preoperative signal-averaged electrocardiogram on left ventricular function after coronary artery bypass graft surgery in patients with left ventricular dysfunction. The CABG Patch Trial.

Patients with ischemic left ventricular (LV) dysfunction often have an improved survival and life quality after coronary artery bypass grafting (CABG), in part due to an improvement in LV function. A lack of LV ejection fraction (EF) improvement postoperatively portends a worse prognosis. Recently, an abnormal preoperative signal-averaged electrocardiogram (SAECG) in patients with a severely depressed LV ejection fraction undergoing elective CABG was shown to be associated with a higher early and late postoperative mortality. The present study evaluated patients with severe LV dysfunction to identify any relation between an abnormal preoperative SAECG and postoperative changes in LV function after successful CABG. Forty-five patients with LV dysfunction (LVEF <0.36) scheduled for elective CABG underwent preoperative SAECG and both pre- and postoperative LVEF determinations using radionuclide scans. Thirty-one patients in the group had an abnormal preoperative SAECG and 14 patients had a normal preoperative SAECG. Baseline patient characteristics were similar in both groups and the mean preoperative LVEF was 0.26. Overall, LVEF improved 31% postoperatively with a significantly greater benefit noted in the group with a normal baseline SAECG (14.9+/-5.7-point vs 4.8+/-8.5-point increase, p <0.001). All patients whose LVEF did not improve or worsened postoperatively had an abnormal preoperative SAECG. No SAECG measure was altered significantly by the operation. A preoperative SAECG provides information on the postoperative functional recovery of ischemic myocardium.

Aged↗
PubMed2004

[Biohumoral markers and right ventricular dysfunction in acute pulmonary embolism: the answer to thrombolytic therapy].

BACKGROUND: Recent data suggest that brain natriuretic peptide (BNP) and troponin I (TnII) are useful markers of right ventricular dysfunction (RVD) and initial myocardial injury in acute pulmonary embolism. The aim of this study was to evaluate biohumoral activation and right ventricular function in patients with acute pulmonary embolism diagnosed at pulmonary scintigraphy. METHODS: We observed 12 patients with massive pulmonary embolism (MPE), 8 with non-massive pulmonary embolism (NMPE) and RVD, 6 with NMPE without RVD. All the patients with MPE and 5 patients with NMPE-RVD received thrombolytic therapy (urokinase or recombinant tissue-type plasminogen activator), the others were treated with heparin. At the beginning and after pharmacological treatment all the 26 patients underwent standard echocardiography and blood test analysis. RESULTS: BNP and Tn1 were significantly high in MPE (BNP p < 0.001 and Tn1I p < 0.005 vs NMPE) and in NMPE-RVD (BNP p < 0.03 and Tnl p < 0.02 vs NMPE). MPE and NMPE-RVD had similar RVD (p = NS), thrombolysis significantly reduced BNP, TnI, systolic pulmonary pressure, both in MPE (p < 0.001) and in NMNPE-RVD (BNP and Tnl p < 0.05, systolic pulmonary pressure p < 0.001). COULSION: Our data sustain the utility of BNP and Tnl as markers of RVD in acute pulmonary embolism; they focus on patients with NMPE-RVD and high levels of BNP and Tnl in whom an aggressive therapy as the thrombolytic one is necessary; they suggest the importance of biohumoral markers as indicators of the efficacy of pharmacological treatment in patients with acute pulmonary embolism.

Acute Disease↗
PubMed2003

Pathological changes of the myocardium in patients after atrial repair for transposition of the great arteries: a possible explanation for left ventricular dysfunction after secondary arterial switch.

BACKGROUND: Patients with transposition of the great arteries who underwent an atrial repair in infancy are likely to develop right ventricular dysfunction later in life. For these patients a two-stage arterial switch operation has been advocated by some groups but mortality even from the initial pulmonary banding procedure for retraining the left ventricle has been reported to be considerable. We asked whether pathological alterations of the left ventricular myocardium could explain for the failure of the left ventricle observed in patients after two-stage arterial switch operations. METHODS: Twelve patients aged 16.9 [8-25.4] years (median [range]) with transposition of the great arteries after atrial repair in infancy were enrolled. Median follow-up interval was 15.8 [7.8-22.1] years. Measurements of right and left ventricular systolic function were performed by echocardiography. In addition all patients underwent cardiac catheterization. Endomyocardial biopsies were taken from the right and left ventricle and examined histopathologically. RESULTS: Two out of twelve patients showed mildly reduced systolic right ventricular function. Systolic function of the left ventricle was normal in all patients on echocardiography but six out of twelve patients showed clusters of fibrous and fatty degeneration on biopsy specimens obtained from the left ventricle. CONCLUSION: We conclude that degenerative left ventricular myocardial changes could serve as an explanation for left ventricular failing when retraining the left ventricle during two-stage arterial switch operations.

Adolescent↗
PubMed2002

[The ECG in prediction of the infarcted artery and left ventricular dysfunction].

OBJECTIVE: To assess the possibilities of ECG in prediction of an infarcted artery in patients with acute myocardial infarction (AIM) and evaluate the relationship of left ventricular function to the number of pathological Qs. METHOD: The trial comprises 216 patients with acute myocardial infarction (AMI) treated by primary PTCA. The diagnosis of AIM was confirmed in addition to ECG also by coronarography and elevation of cardiospecific enzymes. On the baseline 12-lead ECG denivelization of the ST segment > 1 mm was considered significant. The number of pathological Q waves on the ECG tracing on discharge was compared with left ventricular function according to the ejection fraction assessed echocardiographically before discharge. RESULTS: Elevation of ST in leads V1-V4 predicts occlusion of LAD with a sensitivity of 96% and specificity of 69% (p < 0.001 vs. RC segment with a sensitivity of 80% and specificity of 48% (p < 0.001). In inferior AMI the ST elevation in III > II develops in 70% in occlusion of RCA vs. 27% in occlusion of LCX. The mean left ventricular ejection fraction before discharge was in patients with four or fewer pathological Q waves 49 +/- 10% vs. 32 +/- 9% in the presence of pathological Q waves in > 4 leads. CONCLUSION: In patients with AMI according to ECG changes in different leads conclusions may be drawn on the infarcted artery. The presence of pathological Q waves in more than 4 leads predicts severe left ventricular dysfunction.

Angioplasty, Balloon, Coronary↗
PubMed2003

Association of severe coronary stenosis with subclinical left ventricular dysfunction in the absence of infarction.

BACKGROUND: Regional left ventricular (LV) dysfunction may occur in patients with coronary artery disease (CAD) in the absence of infarction, but the causes of this phenomenon are unclear. We sought to identify whether changes in regional LV function were related to stenosis severity, using sensitive new ultrasound markers of function. METHODS: We studied 67 individuals with no history of infarction and with normal LV systolic function: 49 patients with CAD and 18 control subjects without CAD. All patients underwent color Doppler tissue imaging, integrated backscatter (IB), anatomic M-mode echocardiography, and strain rate imaging to detect changes in structure and function. Peak early and late diastolic myocardial velocity, cyclic variation of IB, wall thickness, and percent wall thickening were measured in each basal and mid segment. Strain rate and peak systolic strain were calculated in each wall. CAD was defined as >or=50% diameter stenosis. Normokinetic segments (n = 354) subtended by CAD were divided according to stenosis severity into 3 groups: group 1 (subtended by 50%-69% stenosis); group 2 (subtended by 70%-98% stenosis); and group 3 (subtended by >or=99% stenosis). Each parameter in each group was compared with that in 216 segments from control subjects. RESULTS: Segments subtended by significant CAD showed lower peak early and late diastolic myocardial velocity compared with control segments. Group 3 showed significantly lower myocardial velocities than group 2 for both peak early (4.8 +/- 1.8 vs 6.0 +/- 2.0 cm/s, P <.05) and late (4.5 +/- 2.1 vs 5.6 +/- 2.1 cm/s, P <.05) diastolic myocardial velocity. Group 3 also showed a significantly lower cyclic variation IB than did control segments (6.7 +/- 2.3 vs 7.9 +/- 2.6 dB, P <.05), but there was no difference in calibrated IB, wall thickness, strain parameters, or percent wall thickening. These differences were not attributable to the distribution of segments for patients with severe CAD, nor were they explained on the basis of collaterals. CONCLUSION: Although the absolute values show overlap between groups, the results of this study indicate that subtle changes of regional LV function may occur in the absence of infarction, in association with severe coronary stenoses.

Aged↗
PubMed1999

Cardiomyocytes from hearts with left ventricular dysfunction after ischemia-reperfusion do not manifest contractile abnormalities.

OBJECTIVES: This study evaluated contractile function in cardiomyocytes isolated from hearts with global left ventricular dysfunction following ischemia-reperfusion. BACKGROUND: Ischemia followed by reperfusion is associated with transient contractile dysfunction, termed "stunning." It is not clear whether this phenomenon is primarily due to intrinsic cardiomyocyte contractile dysfunction. METHODS: Global contractile dysfunction was induced in isolated perfused rat hearts (n = 8) using a model of transient global ischemia (20 min) followed by reperfusion (20 min). Hearts perfused uninterrupted for 40 min were used as controls (n = 8). Cardiomyocytes were isolated using enzymatic digestion and were studied under varying degrees of inotropy (using increasing extracellular calcium [Ca2+]o) and loading conditions (varying extracellular perfusate viscosity). Mechanical function was studied with video edge detection and intracellular calcium ([Ca2+]i) kinetics using fura-2 AM. RESULTS: Global ischemia-reperfusion increased left ventricle (LV) end diastolic pressure (450% vs. 33%, p < 0.01) and reduced LV developed pressure (9% vs. 33%, p < 0.01), LV positive (3% vs. 26%, p < 0.01) and negative (5% vs. 33%, p < 0.01) dP/dt. However, cells isolated from these hearts did not manifest contractile dysfunction. In fact, cell shortening (p < 0.0001) and peak rate of cell shortening (p < 0.05) and increase in [Ca2+]i with each contraction (p < 0.024) were higher in these cells during stimulation with [Ca2+]o of 1 to 10 mmol/liter. The EC50 values for calcium dose response and the slope of the relation between change in [Ca2+]i and change in cell length were no different between the groups. Cell loading (with increasing superfusate viscosity from 1 cp to 300 cp) also did not reveal any abnormalities in cells from the hearts subjected to ischemia-reperfusion. CONCLUSIONS: Cardiomyocytes isolated from hearts with ischemia-reperfusion-induced LV dysfunction or "stunning" have normal contractile function and normal [Ca2+]i transients, when studied both in the unloaded and loaded state. Our data suggest that nonmyocyte factors such as abnormalities in extracellular matrix or abnormal myocyte-interstitial tissue coupling may be important for the genesis of cardiac contractile failure in the stunned heart.

Animals↗
PubMed1996

Diabetes mellitus, a predictor of morbidity and mortality in the Studies of Left Ventricular Dysfunction (SOLVD) Trials and Registry.

Diabetes is an independent predictor of morbidity and mortality in patients with symptomatic heart failure, patients with asymptomatic left ventricular dysfunction (defined as an ejection fraction of 35% or less), and in a broader registry population with less stringent entry criteria. Although the SOLVD Trials made a major clinical contribution by proving the value of enalapril, diabetes remains a significant predictor of outcome even after adjusting for treatment with enalapril.

Angiotensin-Converting Enzyme Inhibitors↗