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PubMed1994

[Effects of amrinone on left ventricular function following open heart surgery--analysis with left ventricular pressure volume loops].

The effects of Amrinone on cardiac function soon after extracorporeal circulation (ECC) were studied in 5 patients including mitral valvuloplasty, VSD closure, Fontan operation and coronary AV fistel closure. In all patients, left ventricular volume load decreased postoperatively. To evaluate the efficacy, we obtained left ventricular pressure-volume loops (P-V loop) before and after ECC and after intravenous administration of Amrinone (1 mg/kg) following ECC. P-V loops were produced by measuring left ventricular pressure using a Miller catheter which was retrogradely advanced from the ascending aorta into the left ventricle and by measuring left ventricular diameter to calculate left ventricular volume with Teichholtz' formula. Although no apparent difference of Emax was recognized before and after ECC, Emax increased from 3.2 +/- 2.5 mmHg/cm3 to 5.9 +/- 4.7 mmHg/cm3 after the administration of Amrinone. The left ventricular "systolic" pressure-volume area (PVA) which is the sum of stroke work (SW) and elastic potential energy decreased from 34.4 +/- 16.4 gm to 30.9 +/- 17.8 gm after Amrinone. No difference was also recognized in left ventricular end-diastolic pressure. Ejection fraction increased from 50 +/- 17.5% to 56.1 +/- 17.3%. These results suggested that Amrinone could improve the left ventricular function without prominent change in myocardial oxygen consumption immediately after open heart surgery.

Adult↗
PubMedDate not supplied

Estimation of left ventricular function in patients with a left ventricular assist device.

Patients with profound left ventricular (LV) dysfunction supported by a left ventricular assist device (LVAD) may have recovery of LV function, but current methods for assessing this are difficult or not readily available. A new method to estimate LV performance was tested in 6 patients on LVAD (age, 47 +/- 12 years). Simultaneous measures of LV cross-sectional area (substitute for volume) using transesophageal echocardiographic automated border detection and femoral arterial pressure (substitute for LV ejection pressure) were recorded during brief periods on and off LVAD. During the LVAD off period, femoral arterial pressure and LV area signals were combined on-line to generate arterial pressure-LV area loops. The slope of the linear regression line connecting the end systolic points generated during LV filling after LVAD off was used as an estimate of end systolic elastance denoted by Ees. The average Ees was 3.8 +/- 3.1 mmHg/cm2. These values are significantly lower than those of 13 control patients (22.3 +/- 15.4 mmHg/cm2). This method of estimating Ees may be clinically useful in assessing LV recovery in patients on LVAD after extended support.

Adult↗
PubMed1996

An anti-CD18 antibody limits infarct size and preserves left ventricular function in dogs with ischemia and 48-hour reperfusion.

OBJECTIVES: This study investigated whether an antibody against neutrophil adhesion protein CD18 could limit myocardial infarct size and preserve left ventricular function after prolonged reperfusion in a canine model. BACKGROUND: Myocardial reperfusion injury is mediated in part by accumulation of activated neutrophils. Although antibodies against CD18 have been shown to reduce neutrophil influx and infarct size after ischemia and 3 to 4 h of reperfusion, it is unknown whether protection is sustained beyond this time or whether there is meaningful preservation of ventricular function. METHODS: Dogs undergoing 90-min circumflex coronary artery occlusion and 48-h reperfusion were randomized to receive 1 mg/kg bodyweight of R15.7 (an anti-CD18 antibody, n = 12) or saline (control, n =12) 10 min before reperfusion. Contrast left ventriculography was used to measure left ventricular ejection fraction and regional chord shortening at baseline, during occlusion and at 48 h. Microspheres injected during occlusion were used to measure collateral flow and risk region size. Postmortem infarct size was measured with triphenyltetrazolium chloride. RESULTS: In the dose administered, R15.7 bound to neutrophils in vivo, with >85% saturation of CD18 for >24 h, with sustained antibody excess in the plasma. R15.7 significantly reduced infarct size after adjusting for the effect of collateral flow (p = 0.0002, analysis of covariance). In a subgroup of dogs with collateral flow <30% of nonischemic flow, infarct size was reduced from 34.6 +/- 3.9% (mean +/- SE) of the region at risk in the control group to 19.5 +/- 3.3% in the antibody group (p = 0.008). Ejection fraction and regional chord shortening did not differ between the two groups at baseline or during occlusion, but after 48-h reperfusion, ejection fraction and inferior wall regional cord shortening (representing the infarct zone) were both higher in the R15.7 group than the control group (43.6 +/- 2.9% vs. 28.5 +/- 1.8%, p < 0.01; 2.55 +/- 0.29% vs. 1.06 +/- 0.18%, p < 0.05). CONCLUSIONS: A single injection of an anti-CD18 antibody given before reperfusion can limit myocardial infarct size by nearly 50% and preserve global and regional left ventricular function after 48 h of reperfusion.

Animals↗
PubMed1979

Effect of positive end-expiratory pressure on ventricular function in dogs.

Artificial ventilation with positive end-expiratory pressure (PEEP) reduces venous return by raising intrathoracic pressure. To determine whether PEEP decreases cardiac output further by depressing myocardial function, we constructed Starling curves, using rapid dextran infusion in 7 anesthetized dogs ventilated with zero (ZEEP) and 20 cm PEEP. The changes in stroke volume and in left ventricular stroke work (LVSW) when PEEP was added or removed were significantly greater than could be attributed to the corresponding change in transmural left ventricular end-diastolic pressure (LVEDPTM) on these Starling curves. To the extent that PEEP did not alter left ventricular diastolic volume-pressure characteristics, these data indicated PEEP depressed ventricular function. Identical changes with PEEP in cardiac output (-30%), esophageal pressure (+10 cmH2O), and left ventricular function were observed after pulmonary edema was induced with oleic acid. These results confirm and extend recent suggestions that high levels of PEEP depress left ventricular function in dogs, accounting for about half of the reduction in cardiac output before and during acute pulmonary edema.

Animals↗
PubMed1994

Effect of successful angioplasty following thrombolysis on infarct size and left ventricular function.

The role of the angioplasty following thrombolysis in acute myocardial infarction has been discussed in several studies, however the effect of successful angioplasty on infarct size and left ventricular function has not been properly evaluated. Successful reperfusion was achieved in 79 out of 104 patients with primary anterior acute myocardial infarction. These patients were classified as follows, according to the type of intervention during the acute phase: 50 patients in which thrombolysis was successful (the thrombolysis group); 12 patients who underwent successful immediate angioplasty following successful thrombolysis (the immediate angioplasty group); and 17 patients in which rescue angioplasty was successful (the rescue angioplasty group). The 25 patients whose infarct-related vessels were not reperfused after intervention were classified as the non-reperfused group. Infarct size, evaluated as defect volume by T1-201 SPECT, 1 month after the onset, was 840 +/- 154 units (mean +/- S.D.) in the immediate angioplasty group and was similar to that in the thrombolysis group (948 +/- 88 units), but significantly smaller than in the non-reperfused group (1759 +/- 108 units). There were no significant differences in left ventricular function in the immediate angioplasty group and the thrombolysis group. Successful rescue angioplasty did not have any beneficial effect on left ventricular functions or infarct size, when compared with the failed thrombolytic group (1105 +/- 169 units vs. 1617 +/- 169 units). End-diastolic volume (52 +/- 3 ml/m2) in the successful rescue angioplasty group, however, was significantly smaller than in the failed thrombolysis group (67 +/- 3 ml/m2).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1982

Future applications for the evaluation of ventricular function using echocardiography.

It is almost impossible to anticipate all of the potential technologic and clinical advances in echocardiography; however, the development of new clinical techniques, new instrumentation, stress echocardiography, new contrast agents, the ability to identify tissue types, improved ultrasonics information from the circulating blood. Doppler echocardiography, three dimensional echocardiography, the ability to obtained ultrasonic information using catheters or surgical exploration and especially improved techniques for quantitating echocardiographic data, make the potential usefulness of echocardiography in assessing cardiac function, and specifically left ventricular function, very exciting. We should be able to use the advances in echocardiography to improve our understanding of normal cardiac function and pathophysiology, as well as to enhance our ability to make precise diagnoses.

Computers↗
PubMed1987

Development of congestive heart failure and alterations in left ventricular function in patients with sustained ventricular tachyarrhythmias treated with amiodarone.

The interaction between the efficacy and tolerance of amiodarone and the degree of left ventricular (LV) dysfunction was assessed in 126 patients with sustained ventricular tachyarrhythmias. In all patients radionuclide angiographic LV ejection fraction (EF) was measured before and after 8 to 12 months of amiodarone therapy. At baseline mean EF was 25 +/- 13% and 86 patients had an EF of 30% or less. In patients receiving amiodarone at steady state, there was a small but significant increase in EF (23 to 26%, p less than 0.05). Congestive heart failure (CHF) was present in 43 patients before amiodarone therapy. In 16 patients new (9 patients) or worsened (7 patients) CHF developed during the first year of amiodarone therapy. Development of CHF was not consistently related to a change in EF or heart rate. The clinical efficacy and tolerance of amiodarone were affected by the baseline EF and development of CHF. Efficacy and tolerance was 80% in patients with an EF of more than 30% and 60% in those with an EF of 30% or less. Among the 16 patients in whom new or worsened CHF developed, 6 (38%) died and 9 (56%) had recurrent ventricular tachyarrhythmias. Both baseline EF and development of CHF during amiodarone treatment significantly affect the prognosis in patients with ventricular tachyarrhythmias.

Adult↗
PubMed1982

Two-dimensional echocardiography in predicting left ventricular wall motion abnormalities and left ventricular function.

In an attempt to formulate a reliable noninvasive method of detecting segmental wall motion disturbances, we examined 25 patients with coronary artery disease by two-dimensional echocardiography (2-DE), standard 12-lead electrocardiography (ECG), and biplane left ventriculography. The 2-DE technic predicted qualitative wall motion abnormalities as defined by ventriculography with a sensitivity of 88% and a specificity of 86%. The ECG (Q waves) predicted segmental wall motion disturbances with only 50% and 51% sensitivity and specificity, respectively. Extrapolating the advantages of 2-DE to the assessment of global myocardial function, left ventricular wall motion index (LVWMI) and E-point septal separation (EPSS) by 2-DE were correlated with left ventriculographic ejection fractions; r values were high (.73 and -.76, respectively) in both instances. Thus, 2-DE provides a reliable noninvasive technic by which both regional and global myocardial wall motion disturbances can be assessed. Unlike previous noninvasive methods, the 2-DE results compared very favorably with those of biplane left ventriculography.

Cineangiography↗
PubMed1997

Sphygmomanometrically determined pulse pressure is a powerful independent predictor of recurrent events after myocardial infarction in patients with impaired left ventricular function. SAVE investigators. Survival and Ventricular Enlargement.

BACKGROUND: There is increasing evidence of a link between conduit vessel stiffness and cardiovascular events, although the association has never been tested in a large post-myocardial infarction patient population. METHODS AND RESULTS: We evaluated the relationship between baseline pulse pressure, measured by sphygmomanometry 3 to 16 days after myocardial infarction, and subsequent adverse clinical events in the 2231 patients enrolled in the SAVE Trial. Increased pulse pressure was associated with increased age, left ventricular ejection fraction, female sex, history of prior infarction, diabetes, and hypertension and use of digoxin and calcium channel blockers. Over a 42-month period, there were 503 deaths, 422 cardiovascular deaths, and 303 myocardial infarctions. Pulse pressure was significantly related to each of these end points as a univariate predictor. In a multivariate analysis, pulse pressure remained a significant predictor of total mortality (relative risk, 1.08 per 10 mm Hg increment in pulse pressure; 95% CI, 1.00 to 1.17; P<.05) and recurrent myocardial infarction (relative risk, 1.12; 95% CI, 1.01 to 1.23; P<.05) after control for age; left ventricular ejection fraction; mean arterial pressure; sex; treatment arm (captopril or placebo); smoking history; history of prior myocardial infarction, diabetes, or hypertension; and treatment with beta-blockers, calcium channel blockers, digoxin, aspirin, or thrombolytic therapy. CONCLUSIONS: These data provide strong evidence for a link between pulse pressure, which is related to conduit vessel stiffness, and subsequent cardiovascular events after myocardial infarction in patients with left ventricular dysfunction.

Adult↗
PubMed1984

Improved regional ventricular function after successful surgical revascularization.

Left ventricular segments with reversible asynergy at rest demonstrate reversible myocardial perfusion defects on exercise thallium-201 scintigrams. To determine if improved perfusion eliminates asynergy at rest, 23 patients with angina (stable in 21, unstable in 2) were studied before and after coronary artery bypass surgery. All patients underwent exercise myocardial perfusion scintigraphy, contrast ventriculography and coronary arteriography before and after surgery. Selective graft angiography was performed during the postoperative catheterization to determine graft patency. Segmental ventricular function was quantitated by a regional fraction method. The scintigrams were divided into five regions and compared with the corresponding regions of the ventriculogram. Seventy-one of a possible 142 ventricular segments exhibited exercise-induced perfusion deficits. Preoperative regional ejection fraction was normal in 42 of these segments and abnormal in 29. Postoperatively, in 19 of the abnormal segments, function improved or normalized. All these segments had improved perfusion during exercise after surgery and were supplied by a patent bypass graft. Nine of the 10 segments in which abnormal wall motion persisted postoperatively continued to have exercise-induced perfusion deficits, and 9 of the 10 segments were supplied by an occluded or stenotic graft or one with poor run off. Of the 42 segments with normal wall motion preoperatively, 30 had improved perfusion after surgery and 35 maintained normal function. This study indicates that asynergy at rest is permanently reversed after coronary bypass surgery if improved myocardial perfusion can be documented. These findings are consistent with but do not prove the concept that reversible rest asynergy may reflect chronic ischemia or a prolonged effect from previous ischemic episodes.

Angina Pectoris↗
PubMed2000

[Recovery of left ventricular function after mitral valve replacement for chronic mitral regurgitation: optimal timing of operation according to long-term recovery].

OBJECTIVES: Surgical outcome for mitral regurgitation has significantly improved in recent years, so consideration of the optimal operative timing to achieve long-term quality of life for the patients has become more important. Preoperative indices that predict postoperative left ventricular function are very important for decision of the operative timing. To reassess the optimal operative timing for mitral regurgitation, long-term recovery of the postoperative left ventricular function was correlated with preoperative left ventricular end-systolic volume index(LVESVI). METHODS: One hundred eighty-two patients with mitral regurgitation underwent standard mitral valve replacement between January 1973 and June 1993. The patients were divided into 3 groups according to the preoperative LVESVI: Group I (LVESVI > or = 100 ml/m2) included 23 patients, Group II (60 < or = LVESVI < 100 ml/m2) 81 patients and Group III (LVESVI < 60 ml/m2) 78 patients. Two-dimensional echocardiography was performed to measure left ventricular diastolic dimension, systolic dimension, fractional shortening, end-systolic wall stress and mass index before operation(pre), and 1 month(early) and 3 years(late) after the operation. RESULTS: Left ventricular diastolic dimension in each group decreased in the early period, but Group I returned to the abnormal range in the late period. Left ventricular systolic dimension in Groups I and II was at the upper limit of the normal range in the early period and returned to the abnormal range in the late period, but Group III remained within the normal range throughout the study. Fractional shortening in all groups decreased to the abnormal range in the early period, but only Group III returned to the normal range in the late period. End-systolic wall stress in Group I tended to increase, but Group II had no change, and Group III returned to the normal range during the early and late periods. Mass index in Groups I and II remained within the abnormal range, but Group III returned to the normal range in the late period. CONCLUSIONS: Long-term recovery of the left ventricular function in Group I showed a continuous deterioration due to irreversible change of the left ventricular myocardium and Group II showed no significant change. In contrast, Group III demonstrated a significant improvement after standard mitral valve replacement. Patients with preoperative LVESVI of more than 100 ml/m2 have already lost the optimal timing for surgical treatment of mitral regurgitation.

Chronic Disease↗
PubMed1985

Myocardial metabolism and ventricular function following cold potassium cardioplegia.

Transient alterations in myocardial metabolism and ventricular function were observed after elective coronary bypass grafting despite apparently adequate intraoperative protection with cold potassium cardioplegia. Ninety patients had serial hemodynamic measurements and coronary sinus catheters inserted. Thirty-three patients had thermodilution coronary sinus flow catheters inserted to measure coronary sinus blood flow and to evaluate the myocardial utilization of oxygen and lactate. Nuclear ventriculograms were performed in 43 patients to assess ventricular function. Cardiac index fell after discontinuation of cardiopulmonary bypass and then rose between 2 and 24 hours postoperatively. Myocardial oxygen consumption steadily increased during this period. Myocardial lactate production reverted to lactate extraction 30 minutes after reperfusion. Reactive hyperemia was present during the first 10 minutes after cross-clamp release, and coronary sinus blood flow increased gradually during the first 24 hours postoperatively. The response to the stress of volume loading (the infusion of 250 to 500 ml of a colloid solution) and atrial pacing (at a rate of 110 beats/min) was evaluated 2 to 4 hours postoperatively (EARLY) and between 4 to 6 hours postoperatively (LATE). Volume loading resulted in a decrease in lactate extraction EARLY and an increase LATE (EARLY: -0.07 +/- 0.35 mmol/L; LATE: 0.08 +/- 0.32 mmol/L, mean +/- standard deviation not significant). Atrial pacing resulted in a decrease in lactate extraction EARLY and an increase LATE (EARLY: -0.11 +/- 0.34 mmol/L; LATE: 0.14 +/- 0.36 mmol/L, p less than 0.05). Diastolic compliance (the relation between the end-diastolic volume index) decreased between EARLY and LATE. Systolic function (the relation between the systolic blood pressure and the end-systolic volume index) and myocardial performance (the relation between the left ventricular stroke work index and the end-diastolic volume index) were unchanged. Ejection fraction correlated inversely with the end-diastolic volume index and did not represent an independent index of contractility. After elective coronary bypass grafting and cold crystalloid cardioplegia, myocardial metabolism recovered slowly. Hemodynamic stresses should be avoided in the early postoperative period to prevent progressive ischemic injury.

Adult↗
PubMed1989

Bronchial hyperresponsiveness to methacholine in patients with impaired left ventricular function.

To elucidate the pathogenesis of bronchospasm in congestive heart failure, we studied 23 patients with chronic impairment of left ventricular function due to coronary artery disease or dilated cardiomyopathy. In 21 of them we found marked bronchial hyperresponsiveness to methacholine. The mean dose (+/- SD) of methacholine that elicited a 20 percent decrease in the forced expiratory volume in one second (FEV1) was 421 +/- 298 micrograms, nearly the same as in patients with symptomatic asthma. In contrast, there was no bronchial response to methacholine in 9 of 10 patients who had coronary artery disease but normal left ventricular function. Administration of the bronchodilator albuterol led to a partial (43 percent) reversal of the methacholine-induced bronchial obstruction. In 12 patients, pretreatment with the alpha-adrenergic agonist methoxamine (10 mg by inhalation), a potent vasoconstrictor, fully prevented the methacholine-induced decrease in FEV1. The protective effect of methoxamine was blocked by the alpha-adrenergic antagonist phentolamine in all six patients who received this agent. We conclude that bronchial hyperresponsiveness to cholinergic agonists is frequent in patients with impaired left ventricular function and may contribute to the wheezy dyspnea commonly observed in such patients. The bronchoconstriction may be mediated at least in part by dilatation of the bronchial vessels.

Adult↗