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PubMed2006

Restrictive physiology in cardiogenic shock: observations from echocardiography.

BACKGROUND: Left ventricular diastolic abnormalities are associated with adverse outcome in myocardial infarction. Intra-aortic balloon pump (IABP) support is associated with improved diastolic filling. In the SHOCK trial and registry, average left ventricular ejection fraction (LVEF) was approximately 30%, higher than expected based on the classic paradigm. We hypothesized that restrictive physiology plays a role in cardiogenic shock (CS). METHODS: Echocardiograms obtained during the SHOCK trial within 24 hours of randomization were centrally interpreted. Patients with quantifiable mitral E-wave deceleration time were included (n = 64). The restrictive filling pattern was defined as deceleration time < 140 milliseconds. RESULTS: The restrictive pattern was seen in 60.9% of patients studied. Patients with this pattern had lower LVEF (31.1% vs 39.0%, P = .02) and higher wall motion score index (2.1 vs 1.8, P = .05). Patients with restriction were more likely to have IABP support during echocardiography (73.7% vs 43.5%, P = .03). There was no difference with and without restriction in demographic and hemodynamic variables or in mitral regurgitation degree or extent of coronary disease. The restrictive pattern had positive predictive value of 80% for pulmonary capillary wedge pressure > or = 20 mm Hg. Thirty-day survival was 53.9% with restriction versus 68.0% without restriction, P = .31. There was no difference in New York Heart Association class at 1 year between groups. CONCLUSIONS: The restrictive filling pattern is common in patients with CS, which may suggest that diastolic dysfunction contributes to CS pathogenesis. Patients with the restrictive pattern had lower LVEF despite IABP support. An association between the restrictive pattern and mortality was not demonstrated; power was limited by sample size.

Aged↗

PubMed2005

Left heart failure with a normal ejection fraction: identification of different pathophysiologic mechanisms.

BACKGROUND: Although heart failure with a normal ejection fraction (HFNEF) is a clinically heterogeneous syndrome, a single pathophysiologic mechanism, diastolic dysfunction, is often ascribed to explain this condition. In view of the clinical heterogeneity of these patients, we hypothesized that subgroups of HFNEF patients may have different underlying pathophysiologic mechanisms. METHODS AND RESULTS: Freehand 3-dimensional echocardiography was used to measure left ventricular end-systolic and end-diastolic volumes in 99 asymptomatic normal controls and 2 groups with chronic heart failure: 35 patients with normal ejection fraction with longstanding hypertension (hypertensive HFNEF) and 11 patients with hypertrophic cardiomyopathy without a history of hypertension (nonhypertensive HFNEF). These data, combined with cuff sphygmomanometry and Doppler estimates of LV end-diastolic pressure (EDP) yielded estimated pressure-volume loops and slope (E es,sb ) of the end-systolic pressure-volume relationship, a load independent index of chamber contractility. Nonhypertensive HFNEF patients required high EDPs (21 +/- 2 versus 15 +/- 3 mm Hg in normals, P < .0001) to achieve normal EDVs (98 +/- 25 versus 95 +/- 21 mL in normals, P = NS). Although systolic function (E es,sb ) did not differ from normal, systolic blood pressure was lower than normal in these patients (114 +/- 10 versus 124 +/- 14 mm Hg in normals, P < .05). Hypertensive HFNEF patients also had increased EDP (20 +/- 2 mm Hg), but this was observed at higher than normal EDVs (118 +/- 29 mL, P < .05). Among patients with hypertensive HFNEF, 2 subgroups emerged, 1 with a high E es,sb (4.23 +/- 0.54 versus 2.1 +/- 0.7 mm Hg/mL) and 1 with normal E es,sb (2.31 +/- 0.51 mm Hg/mL). The former group was composed of elderly women with small body size (body surface area 1.7 +/- 0.2 versus 1.9 +/- 0.2 m 2 , P = .02) who had concentrically remodeled ventricles and low stroke volumes. The latter group was more diverse in age, body size, and included patients of both genders with increases in ventricular volumes, stroke volume, and mass consistent with a volume overload state. CONCLUSION: Although HFNEF is commonly thought of as being the result of a single hemodynamic mechanism, these data indicate that subgroups exist with distinctly different underlying pathophysiologies.

Age Factors↗

PubMed1991

Echocardiographic findings in kidney transplanted type 1 (insulin-dependent) diabetic patients with and without a pancreas transplant.

Echocardiography with Doppler recordings was carried out in 14 Type 1 (insulin-dependent) diabetic recipients of pancreas and kidney transplants and in 14 Type 1 diabetic kidney transplanted control patients, matched for age, sex, duration of diabetes, extent of other late complications, time since transplantation, dose of prednisolone, and renal function. HbA1c was 5.5 +/- 0.6 vs 8.7 +/- 1.4% (pancreas transplanted vs kidney only). Both groups had a slight increase in interventricular septum thickness. Left ventricular mass was equal. The ejection fraction as a measure of systolic function was normal and equal, 0.71 +/- 0.05 vs 0.69 +/- 0.07. Diastolic function was also equal in two out of three parameters, isovolumic relaxation time and deceleration time. The A/E ratio, however, tended to be lower in the pancreas transplanted group, 0.94 +/- 0.20 vs 1.06 +/- 0.18 (p = 0.04). This indicates more frequent occurrence of impaired diastolic filling in the recipients of kidney only. Follow-up will show whether diastolic dysfunction increases and may be related to the increased cardiovascular mortality in kidney transplanted Type 1 diabetic patients.

Adult↗

PubMed1989

Changes in right ventricular relaxation during acute anterior myocardial infarction in pigs.

To determine the effect of an anteroseptal myocardial infarction on right ventricular systolic and diastolic function, we studied 12 pigs before and 1 h after left anterior descending coronary artery occlusion. Total arterial occlusion was achieved by the percutaneous, transcatheter placement of a 1 mm Teflon plug into the mid portion of the artery. The resulting infarction involved 28 (SEM 3)% of the left ventricular wall, in the anterior and septal regions. A small rim of the right ventricular free wall adjacent to the septum and the right ventricular apex were also affected. End diastolic pressures in both ventricles rose significantly: left ventricular from 12(1) to 20(2) mm Hg and right ventricular from 8(1) to 10(1) mm Hg. Right ventricular peak systolic pressure increased from 29(2) to 35(2) mm Hg while left ventricular peak systolic pressure did not change. One hour after infarction the half time of isovolumic relaxation of the right ventricle was prolonged from 6.9(0.5) to 8.7(0.4) ms. Ejection fraction in both ventricles was depressed: from 46(1) to 34(2)% in the right ventricle and from 69(3) to 49(3) in the left ventricle. There was no change in either right or left ventricular dP/dt. These data suggest that right ventricular systolic and diastolic dysfunction occurs as the result of an anteroseptal myocardial infarction in pigs.

Acute Disease↗

PubMed2006

Diastolic failure in vascular surgery. A forgotten outcome predictor variable or not?

In vascular surgery, sometimes prediction of surgical outcome prior to surgery is next to impossible despite extensive history, requisite investigations and optimum perioperative management. It is well recognized that the leading cause of death in vascular surgery are cardiovascular events. Each surgeon remembers those patients sustaining morbidity and mortality despite the routine nature of surgery performed and the uncomplicated intraoperative course. In some patients the answer to the etiology regarding this observed poor outcome remains rhetorical and a mystery to be solved. Severity scores depend on the variables used, however if unknown recognized variables are not included, quality measurement of outcome in surgery becomes questionable. As surgeons become charged with evidence-based ideas, clinical observations will remain the child of updating both our own functional equations for outcome for ultimate improvement in patient care. Most patients with isolated diastolic dysfunction as the cause of their symptoms have hypertension or coronary artery disease or both (especially in the presence of renal dysfunction or diabetes mellitus) and can develop symptoms of heart failure in the absence of coronary obstructive picture. But could there be a way of approximating reality when predicting outcome?

Diastole↗

PubMed1997

[The characteristics of cardiac diastolic function in myocardiodystrophy in persons subjected to aromatic hydrocarbon exposure].

Left and right ventricular diastolic function was investigated at doppler echocardiography in patients with myocardiodystrophy exposed to organic aromatic solvents (30 female house painters). The control group consisted of healthy females and females with autonomic-dyshormonal myocardiodystrophy. The study group exhibited diastolic dysfunction characterized by disturbed active relaxation assessed by duration of isometric left and right ventricular relaxation.

Adult↗

PubMedDate not supplied

B-type natriuretic peptide: practical diagnostic use for evaluating ventricular dysfunction.

Assessment of brain natriuretic peptide levels may provide important information that can be used in the evaluation of patients with dyspnea and follow-up of heart failure. Brain natriuretic peptide levels have been shown to be useful for evaluating patients in the emergency department and for evaluating patients complaining of dyspnea in the outpatient setting. Brain natriuretic peptide assessment also provides an adjunct to diagnosis of both systolic and diastolic dysfunction, has prognostic value for heart failure and in acute coronary syndromes, and may be a useful measure to guide therapy. Further work needs to be done to establish the best type of assay to use, to determine the optimal cutoff point for what is considered abnormal, and to determine how conditions other than ventricular dysfunction affect brain natriuretic peptide levels.

Acute Disease↗

PubMed1995

Heart failure with normal systolic function: a common disorder in older people.

OBJECTIVE: To review the incidence, pathophysiology, significance, diagnosis, and treatment of heart failure with normal systolic function in older patients. DATA SOURCE: Scientific reports of diastolic ventricular dysfunction in both the general population and the geriatric population were identified from repeated searches of the MEDLINE database and citations from appropriate articles. STUDY SELECTION: Studies were included only if they demonstrated proper methodology, were from a reputable source, and were published in a peer-reviewed journal. DATA EXTRACTION AND SYNTHESIS: Relevant data were obtained from the articles, with special importance placed on studies designed to examine older patients exclusively or as part of a subgroup in a larger study. Emphasis was placed on data pertaining to the pathophysiology, prognosis, and diagnosis of patients with diastolic dysfunction compared with normals and patients with systolic dysfunction as an etiology of heart failure. Therapeutic interventions were selected for the presence of prospective data with concrete end points such as mortality, functional class, exercise capacity, and regression of left ventricular hypertrophy. CONCLUSION: Diastolic ventricular dysfunction is a significant problem in older people, with at least 40% of older heart failure patients having diastolic dysfunction as the etiology of their heart failure. The pathophysiology of diastolic dysfunction is varied but usually involves impaired left ventricular relaxation and/or increased ventricular stiffness, each partially related to normal aging changes, as well as underlying cardiovascular diseases. The significance of heart failure caused by diastolic dysfunction is great, with increased morbidity and mortality compared with other cardiac diseases that have the same preserved systolic function. Diagnosis of diastolic dysfunction can be clinically difficult and often requires further testing to determine if diastolic dysfunction is present. At this time, no therapy specifically treats diastolic dysfunction, but several medications, such as diuretics, calcium channel blockers, beta blockers, and angiotension-converting enzyme inhibitors, offer symptomatic relief and may prevent progression of the disorder.

Aging↗

PubMed2000

[Echocardiographic follow-up of patients with heart failure. Which parameters should be measured? How often?].

The echocardiographic evaluation keeps a relevant place in the evaluation of patients with heart failure and left ventricular systolic dysfunction, not only for its contribution to the diagnosis, prognostic stratification and comprehension of pathogenetic mechanisms, but also for the analysis of the evolution of the disease and the response to optimal medical therapy. On the other hand, the role of echocardiography in the follow-up of patients with diastolic dysfunction is still unclear. In patients with heart failure and left ventricular systolic dysfunction the analysis of changes in left ventricular function and dimension during follow-up is particularly relevant to recognize the potential benefit of optimal medical therapy with ACE-inhibitors and beta-blockers and their prognostic significance. The echo-Doppler hemodynamic evaluation is also of clinical and prognostic value particularly for the recognition of the persistence or (re)appearance of restrictive filling pattern during follow-up. Moreover, in patients with persistent severe left ventricular systolic dysfunction, the evaluation of right ventricular function may allow for the identification of a subset of patients at high risk for cardiovascular events. A practical flow-chart of echocardiographic assessment of patients with heart failure and left ventricular systolic dysfunction includes the following steps: 1) after 3 to 6 months on optimal therapy, to detect the persistence of restrictive filling pattern, if present at diagnosis; 2) after 12 to 24 months, to analyze the response of left ventricular function and dimension to optimal medical treatment; 3) serial examinations, according to the stage of the disease or to the episodes of worsening heart failure, to identify echocardiographic indicators of disease progression, such as worsening of left ventricular and/or right ventricular function or (re)appearance of restrictive filling pattern. The changes in these parameters seem to have a relevant prognostic significance to define the risk profile of patients with heart failure and left ventricular systolic dysfunction.

Follow-Up Studies↗

PubMed2005

Differences in the immediate effects of smoking on left ventricular diastolic function between healthy volunteers and patients with type 2 diabetes mellitus.

BACKGROUND: In contrast to in-depth studies on the chronic hazardous effects of smoking, the immediate effects of smoking on left ventricular function have not been evaluated in detail. OBJECTIVES: We aimed to assess the hypothesis that smoking a cigarette might have more deleterious immediate impacts on left ventricular function in patients with diabetes mellitus than in healthy volunteers. METHODS: In all, 20 patients with type 2 diabetes mellitus and 25 healthy volunteers were consecutively enrolled. Mitral inflow parameters (peak early and late diastolic velocities, and deceleration time of early diastolic mitral inflow) and mitral annulus velocity parameters (systolic, late, and early diastolic velocity [E']) were obtained together with heart rate and blood pressure before and 5, 15, 30, 45, 60, and 75 minutes after smoking a cigarette. RESULTS: Transient elevations in heart rate and blood pressure were observed after smoking in both groups. In terms of mitral inflow parameters, transient trends toward abnormal relaxation were noted in both groups. For mitral annulus velocity parameters, in contrast to a temporary decrease in E' in healthy volunteers, reduction in E' persisted throughout the study for patients with diabetes. No significant change in peak early diastolic velocity/E' ratio was observed in healthy volunteers; however, a significant increase in peak early diastolic velocity/E' ratio lasted throughout the study period for patients with diabetes. Systolic velocity had no significant change during the study in either group. CONCLUSIONS: Even one cigarette can induce more protracted and more severe left ventricular diastolic dysfunction in patients with type 2 diabetes mellitus than in healthy volunteers. Our results have clinically relevant implications in the current era of increasing recognition of the diabetes epidemic and of the associated cardiovascular risks.

Adult↗

PubMed2004

The heart in systemic sclerosis.

The heart is one of the major organs involved in scleroderma. Cardiac involvement can be manifested by myocardial disease, conduction system abnormalities, arrhythmias, or pericardial disease. Additionally, scleroderma renal crisis and pulmonary hypertension lead to significant cardiac dysfunction secondary to damage in the kidney and lung. This report summarizes the recent advances to further understand the types and mechanism of abnormalities in the heart in scleroderma. New cardiac technology shows significant frequencies of asymptomatic cardiac abnormalities. Further long-term studies are necessary to determine the outcome and the best approach to treatment of such abnormalities. Diastolic dysfunction has been carefully evaluated in scleroderma in recent years and appears to be more common than once realized. There is controversy as to whether this is a significant finding independent to other cardiopulmonary problems. More extensive evaluation of the conduction and the arrhythmia ablative therapy has helped manage these life-threatening complications.

Cardiovascular Diseases↗

PubMed2005

Cardiac, neuroadrenergic, and portal hemodynamic effects of prolonged aldosterone blockade in postviral child A cirrhosis.

OBJECTIVES: The present study was designed to determine the effects of long-term antialdosterone treatment on cardiac structural and functional alterations, portal and systemic hemodynamic as well as adrenergic dysfunction characterizing Child A cirrhotic patients with F1 esophageal varices. METHODS: Twenty-two Child A postviral preascitic cirrhotic patients were randomly allocated to 200 mg/day K-Canrenoate (13 patients, age 59.6 +/- 2.2 yr, mean + SEM) or no-drug treatment (9 patients, age 61.8 +/- 2.3) for a 6-month-period. Measurements, which included hepatic venous pressure gradient (HVPG), left ventricular wall thickness, left ventricular end-diastolic volume and diastolic function (LVWT, LVEDV, and E/A ratio, echocardiography), and muscle sympathetic nerve activity (MSNA, microneurography, peroneal nerve), were obtained at baseline and following 6 months of drug or no-drug treatment. Ten healthy age-matched subjects served as controls. RESULTS: Cirrhotic patients were characterized by increased HVPG, LVWT, and MSNA values and by a depressed E/A ratio. K-Canrenoate treatment significantly reduced HVPG (from 15.3 +/- 1.0 to 13.8 +/- 0.8 mmHg, p < 0.05), LVWT (from 21.8 +/- 0.5 to 20.7 +/- 0.6 mm, p < 0.02), and LVEDV (from 99.2 +/- 7 to 86.4 +/- 6 ml, p < 0.01), leaving E/A ratio and MSNA almost unaltered. No significant change was observed in the untreated group of cirrhotic patients followed for 6 months without intervention. CONCLUSIONS: These data provide evidence that aldosterone blockade by long-term K-Canrenoate administration improves hepatic hemodynamics by lowering HVPG and ameliorates cardiac structure and function by favoring a reduction in LVWT and LVEDV as well. They also show, however, that this therapeutic intervention neither improves left ventricular diastolic dysfunction nor exerts sympathoinhibitory effects.

Adrenergic Fibers↗

PubMed1998

Effects of cardiac versus circulatory angiotensin-converting enzyme inhibition on left ventricular diastolic function and coronary blood flow in hypertrophic obstructive cardiomyopathy.

BACKGROUND: Left ventricular (LV) diastolic function and coronary flow are impaired in hypertrophic obstructive cardiomyopathy (HOCM). This study was designed to evaluate the impact of cardiac and circulatory ACE inhibition on such derangements. METHODS AND RESULTS: Twenty patients with HOCM underwent cardiac ACE inhibition with intracoronary (IC) enalaprilat (0.05 mg/min infused into the left anterior descending coronary artery for 15 minutes) followed by circulatory ACE inhibition with 25 mg sublingual (SL) captopril. Contrast ventriculography, pressure, and coronary flow measurements were performed at baseline, after IC enalaprilat infusion, and 45 minutes after SL captopril. Heart rate was not affected by the respective interventions (75+/-11 versus 76+/-13 versus 75+/-10 bpm; P=NS), whereas mean aortic pressure dropped slightly after IC enalaprilat and significantly after SL captopril (90+/-8 versus 85+/-10 versus 74+/-9 mm Hg; P<.05). Compared with baseline, IC enalaprilat resulted in a decrease in LV end-diastolic pressure (17.6+/-5.9 versus 14.4+/-4.9 mm Hg; P<.05), time constant of isovolumic LV pressure relaxation (tauG) (69+/-9 versus 52+/-10 ms; P<.05), and outflow gradient (45.2+/-6.9 versus 24.4+/-3.7 mm Hg; P<.05) and in an increase in coronary blood flow (107+/-10 versus 127+/-12 mL/min; P<.05) and coronary flow reserve (2.2+/-0.4 versus 2.6+/-0.3; P<.05). After SL captopril, tauG was prolonged (60+/-13 ms; P<.05 versus IC enalaprilat), and LV outflow gradient, coronary blood flow, and coronary flow reserve values returned to baseline (45.5+/-5.3 mm Hg, 107+/-12 mL/min, and 2.2+/-0.5, respectively; P=NS versus baseline). CONCLUSIONS: Activation of the cardiac renin-angiotensin system contributes to LV diastolic dysfunction as well as to the decreased coronary blood flow and coronary flow reserve in HOCM. Cardiac ACE inhibition restores and circulatory ACE inhibition aggravates the above derangements.

Adult↗

PubMed2003

Blood pressure and left ventricular geometric pattern determine diastolic function in hypertensive myocardial hypertrophy.

Abnormal left ventricular (LV) diastolic relaxation is an early sign of hypertensive heart disease. Whether LV diastolic dysfunction is caused directly by raised blood pressure, or by structural changes related to LV hypertrophy remains controversial. We examined 115 hypertensive patients with LV hypertrophy, and two age- and gender-matched groups (38 hypertensive patients without LV hypertrophy and 38 normotensive subjects) by echocardiography to assess determinants of LV diastolic function, and the relation between diastolic function and LV geometric pattern. Diastolic function was evaluated by the E/A-ratio, E wave deceleration time (E-dec), isovolumic relaxation time (IVRT), and the atrioventricular plane displacement method (AV-LA/AV-mean). A multivariate analysis (including gender, age and body mass index) shows diastolic function to be inversely related to blood pressure, LV wall thickness and LV mass, but not to LV end diastolic diameter. The E/A-ratio generally showed the strongest relations. Only the E/A-ratio and AV-LA/AV-mean were related to heart rate. By stepwise regression analysis, age was the strongest determinant for the E/A-ratio, E-dec and AV-LA/AV-mean, followed by systolic blood pressure, heart rate and LV wall thickness. For IVRT, however, LV wall thickness appeared strongest, followed by systolic blood pressure and age. In conclusion, blood pressure and LV wall thickness both have independent influence on LV diastolic function. Age and blood pressure are the most important factors to determine the E/A-ratio and E-dec, whereas LV geometry and blood pressure are most important when IVRT is used. AV-LA/AV-mean may not be useful in hypertensive LV hypertrophy.

Adult↗

PubMed1981

Left ventricular diastolic performance at rest and during exercise in patients with coronary artery disease. Assessment with first-pass radionuclide angiography.

We used first-pass radionuclide angiocardiography to assess filling fraction during the first third of diastole, peak filling rate and peak filling rate during the first third of diastole as indexes of left ventricular diastolic performance at rest and after upright bicycle exercise in 32 normal patients and 68 patients with coronary artery disease. The mean filling fraction was unchanged from rest to exercise in normal patients (47+/- 15% vs 46 +/- 13%; NS). Even in 49 coronary patients with normal (greater than or equal to 50%) ejection fraction at rest, filling fraction was less than that in normal patients at rest (35 +/- 11% vs 47 +/- 15%, p less than 0.001). Despite similar resting heart rates, patients with coronary disease had lower (p less than 0.001) peak filling rate and peak filling rate during the first third of diastole than normal patients. With exercise, filling fraction decreased (p less than 0.001) from the resting value in coronary patients. These data suggest that (1) indexes of diastolic performance can be noninvasively assessed at rest and during exercise using first-pass radionuclide angiocardiography, (2) abnormalities in early diastolic performance are often present at rest in patients with coronary artery disease despite normal systolic performance, and (3) exercise-induced ischemia results in increased early diastolic dysfunction in patients with coronary disease.

Adult↗

PubMed1988

Effects of ouabain and isoproterenol on left ventricular diastolic function during low-flow ischemia in isolated, blood-perfused rabbit hearts.

Myocardial ischemia causes both systolic and diastolic dysfunction. A variety of positive inotropic agents with different subcellular mechanisms may be used clinically in an attempt to reverse ischemic contractile failure. We tested the hypothesis that two inotropic agents, isoproterenol (a beta-adrenergic agonist) and ouabain (a sodium pump inhibitor), might have different effects on left ventricular (LV) diastolic function during ischemic failure despite an equivalent inotropic effect. Isolated isovolumic (balloon-in-LV) blood perfused rabbit hearts were paced at constant physiological heart rate (4 Hz), given either no drug (controls, n = 7), isoproterenol (n = 7), or ouabain (n = 7), and then subjected to 6 minutes of low flow ischemia (75% reduction of baseline coronary flow). The doses of isoproterenol and ouabain were selected to produce equivalent modest inotropic effects (15% increase in LV + dP/dt) in each heart during baseline perfusion conditions. During the ischemic period, there was a marked decrease in contractility, and neither isoproterenol nor ouabain demonstrated a positive inotropic effect relative to the control group. However, these agents had markedly different effects on diastolic chamber distensibility (assessed by end-diastolic pressure at constant LV volume) during ischemia. In the control and isoproterenol groups, diastolic chamber distensibility did not change during the ischemic period. In contrast, ouabain treatment resulted in a marked decrease in diastolic chamber distensibility during ischemia; this change was not completely reversible during the 10-minute reperfusion period. The mechanism by which ouabain decreased diastolic chamber distensibility relative to isoproterenol was assessed indirectly. The ouabain and isoproterenol groups were subjected to equivalent degrees of ischemia as assessed by oxygen supply/demand imbalance; during ischemia, each drug group did not differ with regard to myocardial perfusion rates, determinants of myocardial oxygen demand (heart rate, LV developed pressure, LV + dP/dt), myocardial oxygen consumption, lactate production, and ATP and creatine phosphate content. We therefore inferred that the greater decrease in diastolic distensibility in the ouabain group was not due to a greater metabolic severity of ischemia. These observations are consistent with a mechanism of cytosolic calcium overload induced by ouabain, resulting in persistent active myofilament tension development throughout diastole, to cause the observed decrease in diastolic chamber distensibility during ischemia in the ouabain group.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1988

Serial assessment of left ventricular function following coronary bypass surgery by radionuclide angiocardiography.

The serial change in left ventricular function was investigated by radionuclide angiocardiography in 25 patients undergoing coronary artery bypass grafting (CABG). Multiple gated equilibrium blood pool imaging was performed at rest before, and at 1, 2 and 4 weeks after the operation and also during exercise on a supine bicycle ergometer before and 4 weeks after surgery. Global ejection fraction at rest was unchanged after CABG while peak ejection rate increased significantly at 1 and 2 weeks (p less than 0.01 and p less than 0.05 respectively) after the operation. Peak filling rate at rest was generally unchanged after surgery but peak filling rate during the first third of diastole at rest decreased significantly at 1 and 2 weeks (p less than 0.01 and p less than 0.05). After CABG, the increases in ejection fraction and peak ejection rate with exercise were significantly greater than those values measured before surgery. The increases, due to exercise, in peak filling rate and peak filling rate during the first third of diastole were unchanged after the operation. Radionuclide angiocardiography affords a safe, noninvasive, and highly reproducible procedure for serially assessing ventricular function in patients undergoing CABG. Our study revealed early diastolic dysfunction within 2 weeks of surgery and that CABG abolished abnormalities in left ventricular function induced by exercise.

Aged↗

PubMed1997

Relationship between left ventricular diastolic function at rest and exercise capacity in patients who have suffered a previous myocardial infarction.

To assess whether left ventricular (LV) diastolic function is a determinant of exercise capacity in patients who have suffered a previous myocardial infarction (MI), we investigated the relationship between maximum exercise duration and resting LV diastolic function in 65 MI patients. Each patient underwent both a symptom-limited exercise test and LV biplane angiography with simultaneous high-fidelity pressure measurements. LV relaxation was assessed by the time constants (T1/e and T1/2) of isovolumic pressure decay, and LV diastolic distensibility was assessed by the LV end-diastolic volume (V) index-pressure (P) ratio. The time constants of relaxation did not correlate with maximum exercise capacity (r = -0.19 for T1/e, NS; r = - 0.17 for T1/2, NS). LV diastolic distensibility also did not correlate with exercise capacity (r = - 0.08, NS). These results suggest that the resting LV diastolic dysfunction is unlikely to be the principal cause of exercise intolerance in MI patients without congestive heart failure.

Adult↗