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PubMed1989

Impaired left ventricular functional reserve in hypertensive patients with left ventricular hypertrophy.

To determine whether patients with hypertension and especially those with left ventricular hypertrophy have subtle changes in cardiac function, we measured the increase in left ventricular ejection fraction and in systolic blood pressure to end-systolic volume index ratio with exercise in 40 hypertensive patients and 16 age-matched normotensive volunteers. Twenty-two hypertensive patients without hypertrophy had normal end-systolic wall stress at rest and exercise responses. In contrast, the 18 patients with echocardiographic criteria for left ventricular hypertrophy demonstrated a significant increase in end-systolic wall stress at rest compared with normal subjects (69 +/- 16 vs. 55 +/- 15 10(3) x dyne/cm2, p less than 0.05) despite having normal resting left ventricular size and ejection fraction. In patients with left ventricular hypertrophy, the increase in ejection fraction with exercise was less than in the normotensive control subjects (7 +/- 7 vs. 12 +/- 8 units, p less than 0.05), and delta systolic blood pressure to end-systolic volume with exercise was reduced (3.3 +/- 3.8 vs. 8.3 +/- 7.7 mm Hg/ml/m2, p less than 0.05). The hypertensive patients with hypertrophy displayed a shift downward and to the right in the relation between systolic blood pressure to end-systolic volume ratio and end-systolic wall stress compared with control subjects and hypertensive patients without left ventricular hypertrophy. Thus, hypertensive patients with left ventricular hypertrophy by echocardiography and normal resting ejection fraction exhibit abnormal ventricular functional responses to exercise. This finding may have implications in identifying patients at higher risk for developing heart failure.

Adult↗
PubMed1992

Left ventricular aneurysmectomy in patients with poor left ventricular function.

Physical performance and left ventricular (LV) function in the resting state were assessed in 22 patients with postinfarction anterior-apical left ventricular aneurysm (LVA) and global ejection fraction less than or equal to 20% who subsequently underwent radical LVA resection. The basic findings in the 20 survivors of surgery were significant improvement of global systolic LV function and more or less complete recovery of regional ejection fraction in the predominantly viable low and high lateral LV wall. This improvement was evident in patients with concomitant bypass grafting as well as in those with isolated and ungraftable lesions of the left anterior descending (LAD) coronary artery. We conclude that postinfarction anterior-apical LVA in a poorly functioning LV is suitable for surgical treatment, which can be accomplished with acceptable risk. All graftable stenotic major coronary arteries should be bypassed, in addition to the LVA resection, but a minority of patients with isolated, ungraftable LAD disease are likely to benefit from aneurysmectomy alone.

Adult↗
PubMed1992

Right and left ventricular function in fetal sheep exposed to long-term high-altitude hypoxemia.

To test the hypothesis that long-term hypoxemia affects fetal cardiac function, we measured right (RVO) and left (LVO) ventricular output by electromagnetic flow probes. We also determined their responses to increased preload (ventricular function curve, VFC) and afterload (arterial sensitivity curve, ASC). We exposed seven pregnant ewes to high altitude (3,820 m) from 30 to 120 days gestation, at which time surgery was performed. Thereafter, maternal arterial PO2 was maintained at approximately 60 Torr by N2 administration. Fetal arterial PO2 was significantly reduced in the hypoxemic fetuses (Hyp, n = 7) compared with that of control (Con, n = 9) (19.3 +/- 0.8 vs. 23.3 +/- 0.5 Torr, P less than 0.01). Mean arterial pressures in the Hyp group were elevated (52.0 +/- 1.2 vs. 44.4 +/- 1.7 mmHg, P less than 0.01) and fetal heart rate showed minimal change. Catecholamine concentrations in the Hyp group tended to be higher than the Con group, but not significantly so. For Con and Hyp, RVO equaled 275.7 +/- 9.1 vs. 183.1 +/- 10.1 (P less than 0.01), LVO equaled 165.7 +/- 16.9 vs. 141.6 +/- 16.5 (NS), and combined ventricular output (CVO) equaled 441.1 +/- 22.9 vs. 334.9 +/- 28.3 ml.min-1.kg-1 (P less than 0.05). For the LV there were no significant differences of the VFC between the Con and Hyp groups. However, the right VFC in the Hyp was significantly shifted downward. Concerning afterload, in the RV the slope of the ASC of Con was steeper than that of Hyp (-3.00 +/- 0.05 vs. -0.84 +/- 0.11 ml.ml.min-1.g-1.mmHg-1, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Altitude↗
PubMed1989

Left ventricular function in experimental volume overload hypertrophy.

Left ventricular function in volume overload hypertrophy is controversial. In humans, chronic severe volume overload eventually results in left ventricular dysfunction; paradoxically, experimental volume overload hypertrophy has nearly always been associated with normal left ventricular function. However, in most cases, experimental volume overload hypertrophy has either been mild or only present for a short duration. To help resolve the issue of contractile function in volume overload hypertrophy, we examined ventricular function in a recently described model of severe chronic experimental mitral regurgitation. Left ventricular function was measured before and 3 mo after the creation of severe mitral regurgitation (averaged regurgitant fraction 0.64 +/- 0.04). At 3 mo end-diastolic volume had increased from 78 +/- 5 to 114 +/- 7 ml (P less than 0.01). Significant left ventricular hypertrophy had occurred with an increase in the left ventricular weight-to-body weight ratio from 3.84 +/- 0.2 to 5.22 +/- 0.2 (P less than 0.01). All indicators of left ventricular function (ejection fraction, the end ejection stress-volume relationship, this relationship corrected for eccentric hypertrophy, and mean velocity of circumferential fiber shortening at a common stress) were reduced at 3 mo. Our study produced 64% volume overload which was maintained for 3 mo at which time there was a 36% increase in left ventricular mass. This amount of volume overload of this duration produced significant left ventricular dysfunction.

Animals↗
PubMedDate not supplied

Left ventricular function in patients with centrifugal left ventricular assist device.

We used blood pool radionuclide angiography to study the left ventricular (LV) ejection fraction (EF) in 17 patients with a centrifugal assist device (AD) placed because of severe postoperative LV dysfunction. During maximal LVAD flow, the 12 patients who could be weaned had a higher LV-EF than the 5 who could not be weaned (18 +/- 12% vs. 9 +/- 2%, p = 0.04). Sequential studies during variable AD flows in 12 patients revealed an increase in LV-EF from 15 +/- 7% at maximal flows to 33 +/- 8% during minimal flows (p less than 0.005) in the 10 patients who could be weaned and no change in LV-EF in 2 patients who could not be weaned. The LV-EF during maximal LVAD flow rates was similar in the 10 patients with long-term survival (192 +/- 129 days) and in the 7 patients with only short-term (9 +/- 6 days) survival (LV-EF 17 +/- 12% vs. 12 +/- 6%, p = ns). The long-term survivors, however, had a substantial increase in LV-EF from 20 +/- 13% to 34 +/- 9% (p less than 0.01), as the LVAD flow was decreased from maximal to minimal, whereas the short-term survivors had an insignificant increase in LV-EF from 12 +/- 7% to 21 +/- 12% (p = ns). The long-term survivors increased the LV-EF from maximal to minimal LVAD flows by 182%, in contrast with the short-term survivors, who increased the LV-EF by only 44%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Echocardiographic findings of left ventricular hypertrophy and normalization of parameters of left ventricular function in patients with previous evidence of dilated and poorly contracting left ventricle and coexisting systemic hypertension.

We report 6 cases of dilated left ventricle with poor left ventricular function and coexisting systemic hypertension in whom left ventricular hypertrophy and normalization of left ventricular function and dimensions have been subsequently documented by M-mode and two-dimensional echocardiographic follow-up studies. Four patients were in New York Heart Association functional Class IV, one in Class III, and one in Class II when first seen. Normalization of left ventricular function and dimensions and features of left ventricular hypertrophy (fractional shortening from 15.0 +/- 5.2 to 39.7 +/- 5.4, left ventricular end-diastolic diameter from 6.6 +/- 0.6 to 4.6 +/- 0.6 cm, left ventricular end-systolic diameter from 5.6 +/- 0.8 to 2.8 +/- 0.6 cm, left ventricular end-diastolic radius/posterior wall thickness from 3.1 +/- 0.5 to 2.0 +/- 0.4, interventricular septum thickness from 1.2 +/- 0.3 to 1.5 +/- 0.3 cm, left atrium from 4.6 +/- 0.6 to 3.5 +/- 0.9 cm) were achieved after adequate medical treatment at the end of the follow-up (11-39 months). It appears from this study that normalization of left ventricular dimensions and function with features of left ventricular hypertrophy can occur after adequate treatment in patients with echocardiographic findings of dilated and poorly contracting left ventricle and coexisting systemic hypertension. It is conceivable, in such cases, to classify the dilatation of the left ventricle as secondary and to suggest the hypothesis of a cause-effect relationship between therapy and normalization of left ventricular parameters with findings of left ventricular hypertrophy. Further studies are needed to clarify this phenomenon.

Adult↗
PubMedDate not supplied

Left ventricular function during respiratory failure.

Indirect measures of left ventricular function were studied in seven patients with respiratory failure secondary to chronic obstructive pulmonary disease to determine if there were a relationship between left ventricular function and treatment of the pulmonary disease. All patients were studied during acute episodes while in respiratory failure having arterial Pco2 (Paco2) values greater than 49 torr with no clinical evidence of left ventricular failure. Indirect methods to evaluate left ventricular function included the use of the Swan-Ganz catheter for pulmonary capillary wedge pressure measurement, systolic time intervals, and cardiac output. There was improvement in left ventricular function with treatment of the respiratory failure manifested by decreases in the wedge pressure and pre-ejection period/left ventricular ejection time ratio, and an increase in the dp/dt/pulmonary capillary wedge pressure with treatment of the chronic obstructive pulmonary disease. The improvement in left ventricular function suggests that there is a depression of left ventricular function in respiratory failure. The depressed function improved with therapy of the lung disease without additional medication directed at cardiac function.

Adult↗
PubMed1992

[Coronary artery bypass surgery in patients with severely impaired left ventricular function].

The efficacy and problem of coronary artery bypass grafting (CABG) in patients with severely impaired left ventricular function (left ventricular ejection fraction < or = 30%) were assessed in 27 patients of whom 17 (group 1) underwent emergent CABG and 10 (group 2) elective between Jan 1984 to Aug 1990. As a whole, history of myocardial infarction (24/27, 88.9%), large left ventricular volume with reduced ejection fraction (LVEDVI 126.08 +/- 25.91 ml/m2, LVESVI 93.04 +/- 21.02 ml/m2, LVEF 25.04 +/- 4.75%) and multiple vessel disease with at least one vessel total occlusion (20/27, 74.1%) were characteristically seen in these patients. The patients of group 1 were significantly older (mean 66.12 +/- 5.68 vs 57.10 +/- 8.08, p < 0.01) and needed more frequent preoperative support with IABP (17/17 vs 4/10, p < 0.01). Using Thallium-201 scintigraphy, in 10 patients of group 1 and 9 of group 2, myocardial viability in the proposed bypass area was evaluated before operations. Average 2.37 +/- 0.79 grafts were placed and continuous retrograde cold blood cardioplegia via the coronary sinus was employed for myocardial protection. Two mitral annuloplasty (MAP) for ischemic mitral regurgitation and 2 cryoablation for the treatment of ventricular tachycardia were performed concomitantly. Operative mortality was 47.1% in group 1 and none in group 2 (p < 0.05). Two cases of MAP died, but two cases of cryoablation survived. Postoperative LVEF was improved significantly only in group 2 (p < 0.05), but during the follow-up period of 7 months to 6 years, all 19 survivors expect one remains with NYHA class I or II.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1977

Preclinical abnormaltiy of left ventricular function in chronic alcoholics.

Left ventricular function of a sample of subjects with chronic alcohol intake, in the form of wine, and without clinical or electrocardiographic signs of heart disease was compared with that of a sample of normal control subjects using non-invasive polygraphic recordings. The statistical analysis has shown significant prolongation of PEP, PEPI, an increase in PEP/LVET, and a shortening of LVET and LVETI in the alcoholic subjects compared with the controls. All these abnormalities may be ascribed to left ventricular malfunction.

Adult↗
PubMed1992

[Coronary artery bypass grafting in patients with poor left ventricular function using retrograde continuous cold blood cardioplegia].

Patients with poor left ventricular function or those requiring urgent surgery may have more extensive ischemic myocardial injury if myocardial preservation is incomplete. We have performed coronary artery bypass grafting (CABG) aimed at complete revascularization in such cases using RC-CBCP, which is considered more effective on myocardial preservation during aortic cross-clamping in particular to protect ischemic area distal to severe coronary artery stenosis or obstruction. In the present study, in 25 patients with poor left ventricular function (left ventricular ejection fraction; LVEF less than or equal to 0.3) including 10 patients who required urgent surgery, the operative results were evaluated. All the distal and proximal anastomoses of grafts (average 2.5 grafts) were completed during one aortic cross-clamping using RC-CBCP, therefore graft flow was obtained immediately after release of the aortic clamping. Though this method required 142 minutes of a mean aortic cross-clamping time, myocardial protection was considered to be preferable judging from postoperative isoenzymatic evaluation and improved ventricular function. Fifteen patients with elective CABG were all alive and restored to NYHA class I to II. Among 10 patients requiring urgent CABG, 4 patients with acute myocardial infarction died but others were restored to NYHA class I to II. We conclude that it is important to aim at complete coronary revascularization in patients with poor left ventricular function and RC-CBCP achieves more effective myocardial protection during CABG in the patients.

Adult↗
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↗
PubMed1978

Relationship between maximal oxygen uptake and left ventricular function in exercise.

Left ventricular systolic time intervals (STI's), cardiac output, and arterial blood pressures were measured during bicycle ergometer work in three groups of 10 young men (aged 20-33 yr) who represented average (VO2max = 42-45 ml.kg-1.min-1), moderate (VO2max = 50-56 ml.kg-1.min-1), and high (VO2max = 59-72 ml.kg-1.min-1) levels of cardiovascular fitness. The subjects were studied using noninvasive procedures at steady-state heart rate of approximately 110, 130, and 150 beats.min-1. At all exercise levels, the fitter subjects displayed slightly shorter values for the preejection period (PEP) compared with less fit groups. Significantly (P less than 0.05) larger stroke volumes, longer left ventricular ejection times (LVET), faster mean systolic ejection rates and lower PEP/LVET ratios were found in the group with the highest aerobic capacity. Although these observations appear to indicate a superior mean level of left ventricular performance in groups who represent high levels of cardiovascular fitness, it was concluded that the use of STI values by themselves to describe the cardiovascular fitness of an individual would not be warranted.

Adult↗
PubMed1976

Left ventricular function in chronic renal failure.

Left ventricular function was studied in 14 patients with end-stage chronic renal failure using non-invasive methods (echocardiography and systolic time intervals). Patients were divided into 3 groups. Group 1 consisted of 5 patients who were normotensive at the time of study and group 2 of 7 patients who were hypertensive when studied. Group 3 consisted of 2 patients: one was receiving propranolol and the other, studied 302 days after renal transplantation, was receiving digitalis for recurrent episodes of cardiac failure. All except the patient receiving propranolol had normal left ventricular function in systole with normal measurements of fractional fibre shortening (% delta S, EF) and normal measurements relating to the velocity of ventricular contraction (mean Vcf, mean velocity of posterior wall motion). Stroke volume and cardiac output were normal in some patients but were increased in patients with fluid overload. Early diastolic compliance of the left ventricle seemed to be normal except in the patient with recurrent cardiac failure. The study provided no evidence for the existence of a specific uraemic cardiomyopathy.

Adult↗
PubMedDate not supplied

[Left ventricular function in chronic obstructive lung disease (author's transl)].

Left ventricular function was studied at rest and during post-extrasystolic potentiation in 18 patients with chronic obstructive lung disease. The contractility indices used were obtained from pressures recorded in the isovolumetric period (left ventricular end-diastolic pressure, Vmax., VECmax., dP/dtmax.) and from volume variations during ejection (end-diastolic volume, ejection fraction, VCF). Left ventricular diastolic compliance was also evaluated. All patients were hypoxic (PaO2 = 58 +/- 7 torr); six of them had cor pulmonale (group B); the remaining 12 patients constituted group A. Left ventricular function of groups A and B was similar; we conclude that right cardiac failure, in cor pulmonale, is not secondary to left ventricular failure. However, left ventricular dysfunction exists; the left ventricle is hypertrophied (probably resulting from chronic hypoxia). Pump function is altered (abnormal ventricular function points are found), but left ventricular kinetics is normal or exaggerated (ejection fraction and VCF are increased). Isovolumetric phase contractility indices are diminished; however, they may increase normally during post-extrasystolic potentiation. Left ventricular compliance is abnormal due to left and right ventricular hypertrophy and to paradoxical movement of the interventricular septum which impedes diastolic expansion of the left ventricle. These changes are responsible for decreased left ventricular output. There seems to exist an impairment of left ventricular function related to both intrinsic (secondary to hypoxia, hypercapnia, left ventricular hypertrophy) and extrinsic factors (right ventricula hypertrophy deviating interventricular septum, lowering of left ventricular preload).

Adult↗
PubMed1990

Ultrastructural pathological study of left ventricular myocardium in patients with isolated rheumatic mitral stenosis with normal or abnormal left ventricular function.

An electron microscopic study of left ventricular myocardium was carried out in 15 patients who had isolated rheumatic mitral stenosis, with particular reference to the relation among ultrastructural pathological findings, the severity of mitral stenosis and left ventricular function. They were divided into 2 groups based on left ventricular performance evaluated by 2-dimensional echocardiography and angiocardiography. The severity of mitral stenosis was determined by hemodynamic data and mitral valve areas measured by 2-dimensional echocardiography. Regardless of the level of left ventricular contractile function we consistently demonstrated varying degrees of ultrastructural pathological alterations of left ventricular muscle cells, involving the myofibrils, mitochondria, nuclei and other elements of the sarcoplasm and membranes surrounding the myocardial cells in all specimens examined. The ultrastructural pathological findings did not correlate with the severity of mitral stenosis reflected in the echocardiographic and hemodynamic data. However, those patients with abnormal left ventricular function always exhibited more extensive loss of myofibrils resulting from either disproportion of the mitochondria-to-myofibril ratio or myofibrillar degeneration. The present investigation provides the morphological data at the ultrastructural level to support the widely held concept of a myocardial factor i.e., the extent of myocardial involvement by the rheumatic process as the basic pathogenetic mechanism responsible for left ventricular dysfunction in patients with isolated rheumatic mitral stenosis. Furthermore, it is suggested that pathological alterations of myocardial ultrastructure were related to the extent of myocardial involvement by the rheumatic process rather than being structural adaptations in response to the hemodynamic derangement.

Adult↗
PubMed1991

Effects of nisoldipine on systolic and diastolic function in postinfarction patients with reduced left ventricular function: a randomized, double-blind, placebo controlled study.

The long-term effects of oral nisoldipine or placebo on clinical variables, exercise test results and echo Doppler-determined systolic and diastolic functions were studied in 30 consecutive patients with reduced left ventricular function (predischarge echocardiographic wall motion score greater than or equal to 8) following myocardial infarction. Groups were comparable in clinical variables, exercise results, echo Doppler measurements and coronary anatomy. During 6 months follow-up, death, reinfarction and bypass surgery or balloon angioplasty were equally distributed. A significant increase in exercise duration and time to onset of ST-depression was found in the nisoldipine treatment group, compared to the placebo group after 3 and 6 months. Time to onset of angina was not significantly different. Echocardiographic indices of left ventricular systolic function (ejection fraction and wall motion score) were unaltered; however, the time-velocity integral of the early diastolic filling phase and the early vs late diastolic flow velocity ratio were significantly increased while the atrial time-velocity integral vs total time-velocity integral was significantly decreased in the nisoldipine treatment group after 3 and 6 months of follow-up. In conclusion, nisoldipine reduced exercise-induced ischaemia, improved exercise capacity and diastolic left ventricular function in postinfarction patients with reduced left ventricular function.

Cardiac Catheterization↗
PubMed1976

Normalized first derivative ofthe left apex cardiogram in assessment of left ventricular function.

The relation between the left displacement apex cardiogram and the left ventricular pressure during isovolumic contraction was studied in 30 patients with cardiac disease. Using the instantaneous relation between the first time derivative and the magnitude of both the left apex cardiogram and the left ventricular pressure, normalized derivatives were obtained. These noramized velocities were correlated with each other and with several indexes of left ventricular function. The normalized derivatives of the left apex cardiogram (dD/dt/D) and the left ventricular pressure (dP/dt/P) were similar in magnitude, standard deviation and variation coefficient. No such similarity was present when the first time derivatives of each tracing (dD/dt and dP/dt) were compared. A highly significant relation was found between normalized displacement velocity and normalized pressure velocity using both total (r = 0.76, P less than 0.001) and developed (r = 0.75, P less than 0.001) displacement and pressure. Significant correlations with several other indexes of left ventricular function (end-diastolic pressure, peak dP/dt, maximal velocity of the contractile elements at zero load[Vmax]) were also observed. It is concluded that the index dD/dt/D of the left apex cardiogram is an important noninvasive tool for assessing left ventricular function in man.

Adult↗