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At least 253 records · Page 14Linked to original sources
PubMed2007

Weight loss after bariatric surgery improves aortic elastic properties and left ventricular function in individuals with morbid obesity: a 3-year follow-up study.

OBJECTIVE: To investigate whether weight loss after bariatric surgery (gastric bypass) is associated with changes in aortic function (an important determinant of left ventricular function) and in left ventricular function, in morbidly obese individuals 3 and 36 months after surgery. METHODS: We used echocardiography to evaluate 60 obese individuals [body mass index (BMI) > 40 kg/m2] who underwent surgery and 20 obese individuals who neither underwent surgery nor lost weight, at baseline and at 3 and 36 months of follow-up, and 40 lean individuals (BMI < 25 kg/m2) of similar age, sex and risk factors, at baseline. We measured aortic strain, distensibility, stiffness index, pressure-strain modulus and Doppler indices of left ventricular diastolic dysfunction (ratio of peak early to peak atrial flow velocities, isovolumic relaxation time and deceleration time). RESULTS: Baseline aortic function and Doppler diastolic indices were impaired in obese individuals compared with those who were lean (P < 0.05). During 3 and 36 months of follow-up, BMI and left ventricular diastolic diameter, volume, mass and wall thickness were reduced, and indices of aortic function and left ventricular diastolic function were normalized, in obese individuals after surgery [aortic distensibility (cm2 x dyn(-1) x 10(-6)): 1.9 before surgery, 3.4 at 3 months after surgery and 4.3 at 3 years after surgery, compared with 3.36 in lean controls; P < 0.01], but not in those who did not lose weight. The reduction in BMI after surgery was related to the concomitant improvement in indices of aortic function (P < 0.01) and isovolumic relaxation time (P < 0.05) after adjustment for age, sex and concomitant reduction in blood pressure, lipids and glucose concentrations. CONCLUSION: Weight reduction after bariatric surgery normalizes aortic function, reduces left ventricular hypertrophy and, thus, improves left ventricular diastolic function in morbidly obese individuals over a 3-year period of follow-up.

Adult↗
PubMed1990

Pharmacodynamic effect of nicardipine on left ventricular function in systemic sclerosis.

Left ventricular dysfunction in systemic sclerosis may be due in part to myocardial ischemia caused by a disturbance in coronary microcirculation. We evaluated the pharmacodynamic effect of the calcium channel blocker nicardipine on left ventricular function assessed by radionuclide ventriculography in 20 patients with systemic sclerosis. Resting gated, blood-pool images were obtained at baseline and 90 min after 40 mg of oral nicardipine. The mean (+/- SEM) left ventricular ejection fraction significantly increased from 65.4 +/- 2.3% at baseline to 71.3 +/- 2.3% after nicardipine (p less than 0.005). The mean global defect score significantly decreased from 2.90 +/- 0.73 without nicardipine to 1.50 +/- 0.52 with nicardipine (p less than 0.01). The mean number of left ventricular sectors with severe hypokinesis significantly decreased from 0.80 +/- 0.24 at baseline to 0.20 +/- 0.09 after nicardipine (p less than 0.05). No significant side effects were observed with nicardipine. These results demonstrate short-term improvement in left ventricular function with nicardipine in patients with systemic sclerosis.

Adult↗
PubMed2006

Effects of nebivolol versus carvedilol on left ventricular function in patients with chronic heart failure and reduced left ventricular systolic function.

BACKGROUND: Beta-adrenoceptor antagonist (beta-blocker) therapy results in a significant improvement in left ventricular (LV) systolic function and prognosis in patients with chronic heart failure. Both carvedilol and nebivolol produce hemodynamic and clinical benefits in chronic heart failure, but it is unknown whether their peculiar pharmacologic properties produce different effects on LV function. OBJECTIVE: To assess the effects on LV function of nebivolol compared with carvedilol in patients with chronic heart failure and reduced LV systolic function. METHODS: Seventy patients with a LV ejection fraction <or=40% and in New York Heart Association (NYHA) functional class II or III were randomly assigned to receive carvedilol or nebivolol therapy for 6 months. At baseline and after 6 months of treatment, all patients were assessed clinically and by biochemical and hematological investigation, ECG, 24-hour Holter monitoring, echocardiogram, measurement of ventilatory function, and a 6-minute walk test. RESULTS: Compared with baseline values LV end-systolic volume decreased and LV ejection fraction increased in both the carvedilol (from 79 +/- 38mL to 73 +/- 43mL and from 33% +/- 6% to 37% +/- 11%) and the nebivolol group (from 72 +/- 35mL to 66 +/- 32mL and from 34% +/- 7% to 38% +/- 10%), although the between-group differences were not statistically significant. ECG data showed a decrease in resting HR in both groups (from 83 +/- 20 bpm to 66 +/- 11 bpm for carvedilol and from 81 +/- 15 bpm to 65 +/- 11 bpm for nebivolol; p < 0.001 vs baseline for both groups) but no difference in the PQ, QRS, and QT intervals. Hematologic (in particular, N-terminal pro-brain natriuretic peptide), Holter monitoring (with the exception of HR), and respiratory functional data did not show any significant variation in either group after 6 months' therapy. SBP and DBP decreased in both groups. A small reduction in mean NYHA functional class from baseline was seen in both groups (from 2.5 +/- 0.5 to 2.2 +/- 0.5 for carvedilol [p < 0.05] and from 2.3 +/- 0.4 to 2.2 +/- 0.5 for nebivolol [not significant]). The 6-minute walk test showed a trend toward an increase in the walking distance in both groups. During 6 months of treatment no significant differences in adverse events were observed between the groups. CONCLUSION: Nebivolol is as effective as carvedilol in patients with symptomatic chronic heart failure and reduced LV systolic function.

Adrenergic beta-Antagonists↗
PubMed1990

[Somatostatin and ventricular function in liver cirrhosis].

Left ventricular function is studied in cirrhotic patients and in patients with alcoholic hepatitis by means of isotopic ventriculography (Tc99m) both in basal conditions and after the i.v. injection of a somatostatin bolus (250 mcg). The results obtained are compared to those of conventional hemodynamics. Basal ventricular function is normal in both groups and somatostatin induces a significant decrease (p less than 0.001) in heart rate (74 + 12 vs 67 + 11 bpm), ejection fraction (60 + 6 vs 57 + 65) and maximal ejection rate (-3.3 + 0.4 vs -2.0 + 0.3) in patients and normal controls respectively. The hormone induces a significant increase (p less than 0.01) in telediastolic pressure of the left ventricle (8.1 + 4 vs 21 + 7 mmHg) with no change in systemic resistance. The results suggest that somatostatin has a negative inotropic effect on the heart as well as causing bradycardia.

Adult↗
PubMed1992

Effects of external constraint on the fetal left ventricular function curve.

To determine if external ventricular constraint significantly limits fetal left ventricular (LV) stroke volume and can thus account for the plateau of the fetal ventricular function curve, we studied nine fetal lambs (142 to 144 days' gestation) after partial delivery by cesarean section (halothane anesthetic). LV stroke volume (electromagnetic flow probe), LV end-diastolic pressure, and external ventricular constraint (intrapericardial pressure [liquid-filled balloon]) were measured over a range of end-diastolic pressures under two conditions: with a closed chest and closed pericardium and with an open chest and open pericardium. Stroke volume recorded during open chest and open pericardium exceeded those recorded during closed chest and closed pericardium at any given end-diastolic pressure (p less than 0.01). Decreases in external ventricular constraint significantly increased LV transmural pressure (preload) and substantially increased fetal LV stroke volume. Thus the plateau of the fetal ventricular function curve was largely a result of external ventricular constraint limiting LV preload, not necessarily a result of myocyte immaturity.

Animals↗
PubMed1996

Recovery of systolic and diastolic left ventricular function early after cardiopulmonary bypass.

BACKGROUND: Impairment of left ventricular function after cardiopulmonary bypass (CPB) is well recognized, but little is known about the time course of recovery of cardiac function early after separation from CPB. Therefore, recovery of left ventricular function was evaluated early after separation from CPB in patients undergoing coronary artery surgery. The authors tried to determine whether this recovery might be attributed to autoregulation of function by preload. METHODS: Left ventricular pressure was measured with fluid-filled catheters. Data were digitally recorded during increased pressure induced by elevating the legs. Transgastric short-axis echocardiographic views of the left ventricle were simultaneously recorded on videotape. Systolic function was evaluated with the slope (Ees, mmHg/ml) of the systolic pressure-volume relation. Diastolic function was evaluated with the chamber stiffness constant (Kc, ml-1) of the diastolic pressure-volume relation. Cardiac function was assessed before CPB, after termination of CPB, and 5, 10, and 15 min later. Two different separation procedures from CPB were compared: in protocol 1, left ventricular function was documented during the standard procedure (n = 24); in protocol 2, the heart was optimally filled 10 min before separation from CPB (n = 12). RESULTS: In protocol 1, Ees was 2.88 +/- 0.21 mmHg/ml (mean +/- SEM) and Kc was 0.012 +/- 0.001 ml-1 before CPB. Within 10 min after separation from CPB, Ees increased from 1.10 +/- 0.32 to 2.92 +/- 0.34 (P = 0.001) and Kc decreased from 0.022 +/- 0.002 to 0.011 +/- 0.001 (P = 0.001). The parameters remained stable thereafter. In protocol 2, Ees was 2.92 +/- 0.51 mmHg/ ml and Kc was 0.011 +/- 0.002 ml-1 before CPB. Depression of systolic and diastolic function was not observed in these patients. At time 0, Ees was 2.46 +/- 0.16 and Kc was 0.012 +/- 0.002. These values remained stable throughout the entire observation period. CONCLUSIONS: Significant functional recovery was observed early after separation from CPB, which was suggestive of time-dependent changes in both systolic and diastolic left ventricular function induced by preload restoration.

Anesthesia↗
PubMed2003

Aortic valve replacement in patients with impaired ventricular function.

BACKGROUND: Patients with reduced ventricular function undergoing aortic valve replacement have increased operative risks, but the impact of valvular pathophysiology and other risk factors has not been clearly defined. METHODS: From June 1992 through June 2002, 1,402 consecutive patients underwent isolated aortic valve surgery with or without coronary artery bypass grafting; of these patients, 416 had an ejection fraction less than 40% and are the subject of this report. These patients (mean age, 68.6) had severe stenosis (62.5%), severe regurgitation (30.3%), or mixed disease (7.2%). Aortic valve replacement plus coronary artery bypass grafting was performed in 48.4% of patients, and 27% had previous cardiac surgery. Follow-up included echocardiography and survival analysis. RESULTS: Hospital mortality was 10.1% (42 of 416), with no difference between aortic stenosis (9.6%) and regurgitation (11.1%). Multivariate analysis revealed that age (p = 0.002) and renal disease (odds ratio = 4.2; 95% confidence interval, 1.9 to 9.3; p = 0.001) were independently associated predictors of mortality. Valvular pathophysiology had no impact on mortality. Peripheral vascular disease, multivessel coronary disease, and renal disease were associated risks for any postoperative complication. Peripheral vascular disease (odds ratio = 12.3, p = 0.02), history of cerebrovascular disease (odds ratio = 4.8, p = 0.038), and diabetes (odds ratio = 2.7, p = 0.04) were associated risks for stroke. The ejection fraction was more than 40% in 52% of the patients who had postoperative echocardiography (mean follow-up, 6 months). Actuarial survival revealed no difference between pathophysiologic groups. CONCLUSIONS: Aortic valve surgery in patients with impaired ventricular function carries an acceptable operative risk that can be stratified by age and comorbidities. The type of valvular pathophysiology does not significantly affect mortality.

Aged↗
PubMed1997

Influence of left ventricular function on survival after coronary artery bypass grafting.

BACKGROUND: Preoperative left ventricular function is a most important predictor for survival in patients with ischemic heart disease. To elucidate the optimal timing of recommended coronary artery bypass grafting, we investigated the influence of different aspects of preoperative left ventricular function on relative survival. METHODS: To calculate the relative survival and estimate the disease-specific survival, we compared 6,514 patients who survived the first month after primary coronary artery bypass grafting with the general Swedish population stratified by age, sex, and 5-year calendar period. In particular we studied the relation between relative survival and different aspects of left ventricular performance, namely left ventricular function at rest, New York Heart Association functional class, and number of previous myocardial infarctions. RESULTS: The three variables (left ventricular function at rest, New York Heart Association functional class, and number of previous myocardial infarctions) as well as age and follow-up year gave independent information concerning relative survival. The results from this multivariate analysis were used to define a risk score for each patient. Patients were categorized into different risk groups. Patients in the low-risk group (30% of the total) showed a survival better than that of the population at large for 9 years after operation. The medium-risk group had no or low excess mortality for about 7 years, and the high-risk group (25%) showed increased excess mortality immediately after operation. CONCLUSIONS: If primary coronary artery bypass grafting is performed before the left ventricular function and physical performance deteriorate, survival is excellent.

Actuarial Analysis↗
PubMed1992

Effects of acute, transient coronary occlusion on global and regional right ventricular function in humans.

OBJECTIVES: The aim of this study was to investigate the changes in right ventricular function during acute coronary occlusion produced by inflating a coronary angioplasty balloon catheter. BACKGROUND: Alterations in right ventricular function are well known to occur in patients with acute myocardial infarction or ischemic cardiomyopathy. However, the changes in right ventricular function resulting from acute, transient coronary occlusion of each of the major coronary arteries have been scantily studied, perhaps because of serious limitations of currently available technology. METHODS: A newly designed, mobile, multiwire gamma camera, in combination with generator-produced tantalum-178, affords high count rate first-pass radionuclide angiography and is thus ideal for studying right ventricular function at the bedside. Accordingly, 46 patients underwent first-pass radionuclide angiography at baseline and during transient coronary occlusion induced by a coronary angioplasty balloon catheter. RESULTS: A significant, albeit modest, decrease in global right ventricular ejection fraction occurred during occlusion of the left anterior descending (from 42.9 +/- 9.3% to 39 +/- 8.7%, p < 0.05) and left circumflex (from 44 +/- 9.1% to 38.8 +/- 7.9%, p = 0.03) coronary arteries, but diagonal artery occlusion caused no significant change in right ventricular ejection fraction. Occlusion of the right coronary artery proximal (but not distal) to the acute marginal branch caused a significant decrease in right ventricular ejection fraction (from 42.6 +/- 4.7% to 35.7 +/- 7.2%, p < 0.01). Although occlusion of the left anterior descending, left circumflex and proximal right coronary arteries all caused significant deterioration in regional right ventricular function, only proximal right coronary occlusion caused right ventricular dilation (p < 0.005). CONCLUSIONS: Significant impairment of right ventricular function occurs during transient occlusion of the left anterior descending, left circumflex and proximal right coronary arteries, but only occlusion of the latter causes acute right ventricular dilation, probably as a result of ischemia.

Adult↗
PubMed2002

Physiological changes in ventricular filling alter cardiac electrophysiology in patients with abnormal ventricular function.

OBJECTIVE: To explore the hypothesis that patients with abnormal ventricular function have an altered electrophysiological response to physiological changes in ventricular filling which is not evident in people with normal ventricles. DESIGN: The influence of an acute alteration in ventricular filling on dispersion of repolarisation, measured as QT dispersion, was examined in subjects with normal (n = 9) and abnormal ventricles (n = 9). A physiological reduction in ventricular filling was achieved using dual chamber atrioventricular (AV) pacing in two different modes-AV pacing: atrial activation 120 ms before ventricular activation such that atrial contraction occurred normally in late diastole; and VA (ventriculoatrial) pacing: atrial activation 50 ms after ventricular activation, such that atrial contraction occurred after closure of the AV valves. The absence of effective atrial contraction was confirmed by echocardiography. Ventricular cycle length and sequence of excitation through the ventricle was constant throughout both VA and AV sequences within each patient. RESULTS: During AV pacing (normal ventricular filling) there was no significant difference in QT dispersion between the two groups. In contrast during VA pacing, when the atrial component to ventricular filling was abolished, there was an immediate and consistent increase in QT dispersion compared with baseline in subjects with abnormal ventricular function (p < 0.001) but not in those with normal ventricles. CONCLUSIONS: An abrupt change in ventricular filling, within the physiological range, increased QT dispersion in subjects with abnormal ventricular function but not in subjects with normal ventricles. The findings suggest an altered electrophysiological response to ventricular load in patients with abnormal ventricular function.

Echocardiography↗
PubMed2003

A single intravenous dose of ivabradine, a novel I(f) inhibitor, lowers heart rate but does not depress left ventricular function in patients with left ventricular dysfunction.

This randomized, single-blind, placebo-controlled study investigated the effect of ivabradine, a novel heart rate-lowering agent, on echocardiographic indices of left ventricular (LV) systolic function in patients with regional (coronary artery disease) or global (cardiomyopathy) LV dysfunction. Patients were randomized on an unequal basis to receive ivabradine 0.25 mg/kg (n = 31) or placebo (n = 13) by intravenous infusion. Resting heart rate was reduced by a mean of 17.6 +/- 4.7% with ivabradine and 1.5 +/- 5.8% with placebo. The mean maximum decrease in LV ejection fraction was 0.2% with ivabradine and 1.7% with placebo. Fractional shortening and stroke volume were also fully preserved after ivabradine administration. Thus, a single intravenous dose of ivabradine produced a substantial reduction in resting heart rate without affecting LV function in patients with regional or global LV dysfunction.

Adult↗
PubMed1993

Left ventricular function after coronary artery reperfusion.

Left ventricular dysfunction and dilation after reperfusion relate to the amount of infarcted and dysfunctional myocardium and will continue to be important determinants of morbidity and mortality. There is marked heterogeneity in the anatomic and pathophysiologic presentation of patients with acute myocardial infarction prior to thrombolysis, and many of these individual settings resemble those in animal species with various degrees of collateral formation. Three major determinants of infarct size are responsible for this heterogeneity and include the risk area, the duration of the coronary occlusion, and the level of the residual coronary blood flow via collaterals or a partially patent artery. All 3 of these determinants will influence the initial and late results of reperfusion therapy on infarct size and ventricular function. However, in addition to late or unsuccessful thrombolysis, there are other important factors determining outcome: inadequate reflow, residual coronary stenosis, and coronary reocclusion, factors that can be associated with late progressive left ventricular dilation and dysfunction. The risk factors for left ventricular dysfunction and dilation after reperfusion can now be identified, and such patients should undergo coronary angiography prior to hospital discharge and, if appropriate, revascularization of the infarct-related artery (and perhaps other vessels). In other patients, if serial studies reveal progressive left ventricular failure and dilation late after reperfusion, despite therapy with an angiotensin-converting enzyme (ACE) inhibitor, and if repeat coronary angiography identifies significant coronary stenoses and areas of hibernating or stunned myocardium, revascularization may limit progression of dilation and improve left ventricular function.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Effects of altered PaO2 and PaCO2 on left ventricular function and coronary hemodynamics in sheep.

The effects of acute changes in arterial carbon dioxide and oxygen tension, produced by altering the inspired gas mixtures while maintaining constant-volume intermittent positive pressure ventilation, on global function, regional left ventricular function, and coronary hemodynamics were studied in eight sheep during halothane anesthesia. Hypercapnia (Paco2, 73.5 +/- 2.3 mm Hg, mean +/- SD) increased heart rate, stroke volume, and cardiac output but decreased systolic shortening in the base of the left ventricle. Hypocapnia (PaO2, 24 +/- 1.5 mm Hg) decreased cardiac output and coronary flow below levels seen with hypercapnia but not below levels seen with normocapnia. Systolic shortening decreased in both apical and basal regions, and left ventricular relaxation was impaired as evidenced by a reduction of the nadir of LV dP/dt. Hypoxemia (PaO2, 39 +/- 1.5 mm Hg) elicited a hyperdynamic response of the circulation, increased coronary blood flow, and exhausted the coronary flow reserve. Neither changes in PaCO2 nor changes in PaO2 caused postsystolic shortening, although hypercapnia caused nonuniformity of contraction in the left ventricle. Thus, marked alterations in oxygen and carbon dioxide tensions do not cause left ventricular dysfunction, even though moderate hypoxia reduces the coronary flow reserve.

Anesthesia, Inhalation↗
PubMed1970

Experimental myocardial infarction. II. Acute depression and subsequent recovery of left ventricular function: serial measurements in intact conscious dogs.

Acute myocardial infarction causes depression of left ventricular function, but the capacity of the ventricle to recover from such an injury remains unknown. This problem was explored by measuring left ventricular function in eight intact conscious dogs before, 1 hr after, and again 6-8 days after myocardial infarction. Acute myocardial infarction was produced using a technique which entails gradual inflation over an average period of 1 hr of a balloon cuff previously implanted around the left anterior descending coronary artery. Occurrence of anterior wall infarction was detected electrocardiographically and later confirmed by postmortem examination. Left ventricular function was evaluated from the relationship between left ventricular developed pressure (left ventricular peak systolic pressure minus left ventricular end-diastolic pressure) and left ventricular end-diastolic pressure during transient aortic occlusion with a balloon catheter. Left ventricular function curves were obtained by plotting left ventricular-developed pressure at increasing left ventricular end-diastolic pressures up to 50 mm Hg. Acute myocardial infarction caused marked depression of left ventricular function measured 1 hr after onset of infarction, but 1 wk later all eight animals showed improvement with return of function toward the control levels. A small but significant descending limb was noted at left ventricular end-diastolic pressures above 35 mm Hg. Quantitatively, the descending limb was similar before, 1 hr after, and 1 wk after myocardial infarction. Hemodynamic data revealed evidence of left ventricular failure in all animals, but variability in individual hemodynamic parameters was noted. The data indicate that the marked depression of left ventricular function observed immediately after experimental acute myocardial infarction undergoes considerable resolution within 1 wk, but that functional recovery remains incomplete.

Acute Disease↗
PubMed2005

Effect of rate and rhythm control on left ventricular function and cardiac dimensions in patients with persistent atrial fibrillation: results from the RAte Control versus Electrical Cardioversion for Persistent Atrial Fibrillation (RACE) study.

OBJECTIVES: The purpose of this study was to evaluate left ventricular function and atrial and ventricular diameters in patients with persistent atrial fibrillation (AF) treated with rate or rhythm control. BACKGROUND: Restoration of sinus rhythm in patients with persistent AF may improve left ventricular function and reduce atrial dimensions. Adequate rate control in AF may preserve ventricular function. METHODS: In 335 patients included in the RAte Control versus Electrical Cardioversion for Persistent Atrial Fibrillation (RACE) study, echocardiography was performed at baseline and 1- and 2-year follow-up. Echocardiography was compared between patients randomized to rate control (n = 160) and rhythm control (n = 175). In the rhythm control group, echocardiography was compared between patients with AF versus sinus rhythm at study end. Multivariate analysis was performed to determine parameters related to improvement of left ventricular function and increase of atrial diameters. RESULTS: Fractional shortening improved significantly under rate and rhythm control (31 +/- 10% at baseline to 33 +/- 9% at 2 years, and from 30 +/- 10% to 34 +/- 9%; both P < .05, respectively). Under rate control, left and right atrial size increased significantly compared to baseline. Under rhythm control, only left atrial size increased. Multivariate analysis revealed that only sinus rhythm at study end was associated with an increase of fractional shortening. AF at study end, hypertension, and no use of angiotensin-converting enzyme inhibitors were independently associated with increase in atrial size. CONCLUSIONS: Routine rate control prevents deterioration of left ventricular function. Maintenance of sinus rhythm is associated with improvement of left ventricular function and reduction of atrial sizes.

Aged↗
PubMed2005

Assessment of percutaneous coronary intervention on regional and global left ventricular function in patients with chronic total occlusions.

BACKGROUND: The improvement of regional and global ventricular function following percutaneous coronary intervention (PCI) with reperfusion of the artery supplying the infarct area in acute myocardial infarction is well-described. However, little is known of the potential effects of late recanalization of chronic coronary artery occlusion on left ventricular function. OBJECTIVE: To determine whether PCI improves regional and global left ventricular function in patients with chronic coronary artery occlusions. PATIENTS AND METHODS: Thirty-five patients having at least one coronary artery occluded for six weeks or longer were included in the present prospective study. Exercise thallium-201 myocardial perfusion scintigraphy, multiple-gated acquisition ventriculography and two-dimensional echocardiography were performed in 19 patients (16 men; mean age of 58+/-5 years) who underwent a successful PCI to assess both regional and global left ventricular function before and six weeks following the procedure. RESULTS: The mean ejection fractions before and after reperfusion were 51+/-7% and 58+/-6% using Simpson's method (P<0.001) by echocardiography, and 45+/-1% and 53+/-1% (P=0.01) by multiple-gated acquisition ventriculography, respectively. The echocardiographic wall motion score was 24+/-9 before and 15+/-6 after PCI (P<0.001). The exercise perfusion score (21+/-1 and 14+/-1 [P=0.01]), rest perfusion score (15+/-1 and 12+/-1 [P=0.02]) and reinjection perfusion score (14+/-1 and 11.1+/-1 [P=0.07]) also improved after PCI. The presence of angina was strongly associated with an improvement in left ventricular function and wall motion score (P<0.01). CONCLUSIONS: PCI significantly improved the regional and global left ventricular function in patients with chronic total coronary occlusion. This procedure may provide symptom benefits in selected patients.

Angina Pectoris↗
PubMed1980

Left ventricular function in chronic obstructive pulmonary disease.

Left ventricular function was studied at rest and during post-extrasystolic potentiation (PESP) in 18 patients with chronic obstructive lung disease. The contractility indices were obtained from pressures recorded in the osovolumetric period and from volume variations during ejection. All patients were hypoxic; six of them had cor pulmonale (group B); the remaining 12 patients constituted group A. Left ventricular function was similar in both groups; it is concluded that right heart failure in cor pulmonale is not secondary to left ventricular failure. Left ventricle was hypertrophied and pump function altered, but left ventricular kinetics was normal or increased. Isovolumetric phase contractility indices were decreased; they may increase during PESP. Left ventricular compliance was altered due to left and right ventricular hypertrophy and to paradoxical movement of interventricular septum which impeded diastolic expansion of left ventricle. The impairment of left ventricular function seems to be related to both intrinsic (hypoxia, hypercapnia, hypertrophy) and extrinsic factors (right ventricular hypertrophy with deviation of interventricular septum, lowering of left ventricular preload).

Adult↗
PubMedDate not supplied

Evaluation of right ventricular function during clinical left ventricular assistance.

Hemodynamic and mechanical parameters of right ventricular (RV) performance were measured in eight patients undergoing left ventricular (LV) assistance as a bridge to cardiac transplantation. All patients, even those with impaired RV performance, survived support and transplantation. The reduction of LV afterload produced by the left ventricular assist system (LVAS) results in RV afterload reduction, which permits even the marginal RV to function adequately during LVAS support.

Adult↗