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PubMed1992

Regional left ventricular wall thickening. Relation to regional uptake of 18fluorodeoxyglucose and 201Tl in patients with chronic coronary artery disease and left ventricular dysfunction.

BACKGROUND: In previous studies comparing regional 201Tl (201Tl) and 18fluorodeoxyglucose (FDG) activity in patients with chronic coronary artery disease and left ventricular dysfunction, we hypothesized that regions with mild-to-moderate reduction in FDG activity and regions with mild-to-moderate irreversible 201Tl defects after 3- to 4-hour redistribution represent viable myocardium. In the present study, regional FDG and 201Tl activities were compared with regional systolic wall thickening by gated magnetic resonance imaging (MRI) to confirm the presence of viable myocardium in these territories. METHODS AND RESULTS: Twenty-five patients with chronic stable coronary artery disease and left ventricular dysfunction (ejection fraction, 28 +/- 10) underwent exercise 201Tl tomographic imaging (SPECT), using a reinjection protocol, positron emission tomography (PET) with FDG and H2(15)O, and gated MRI. Matched SPECT, PET, and MRI tomograms were analyzed. From the PET data, 105 regions had matched reduction in FDG and blood flow, of which 69 regions had moderately reduced FDG uptake (50-79% uptake relative to a normal reference region) and 36 had severely reduced FDG uptake (less than 50% of normal activity). Regions with moderately reduced as compared with severely reduced FDG activity had greater end-diastolic wall thickness (9.4 +/- 2.6 versus 8.0 +/- 3.7 mm; p less than 0.05) and regional systolic wall thickening (1.7 +/- 2.7 versus -0.7 +/- 2.1 mm; p less than 0.01). From the SPECT data, 169 irreversible 201Tl defects after 3-4 hour redistribution were identified, of which 70 were mild (greater than 65 to less than 85% of maximal 201Tl activity), 52 were moderate (50-65% of maximal activity), and 47 were severe (less than 50% of maximal activity). Regional systolic wall thickening was greater in regions with normal 201Tl uptake (3.3 +/- 2.3 mm) as compared with all other regions. Regions showing only mild or moderate irreversible defects at redistribution, however, showed wall thickening (2.4 +/- 2.4 and 2.2 +/- 2.5 mm, respectively), which was similar to that observed in regions with reversible 201Tl defects (2.1 +/- 2.2 mm). Only regions with severe irreversible defects at redistribution showed absence of thickening (-0.1 +/- 2.9 mm, p less than 0.01 versus all other groups). After 201Tl reinjection, 12 of 47 (26%) regions with severe irreversible defects showed enhanced 201Tl uptake. The impairment in regional systolic wall thickening was not significantly different between 201Tl defects with and without enhanced 201Tl uptake after reinjection. FDG activity, however, was present in all 12 regions (100%) with enhanced 201Tl uptake after reinjection as compared with only five of 35 (14%) that were unchanged after reinjection (p less than 0.01). CONCLUSIONS: Therefore, preserved wall thickness and systolic wall thickening in regions with moderate reduction in blood flow and FDG activity, and in irreversible 201Tl defects that are only mild-to-moderate, provide additional evidence that such regions represent viable myocardium. Moreover, the finding of metabolic activity and 201Tl uptake in regions with reduced blood flow and absent wall thickening provides clinical evidence of hibernating myocardium in humans.

Adult↗
PubMed1986

Effects of esmolol on patients with left ventricular dysfunction.

This study examined the effect of esmolol, an ultrashort-acting beta-receptor blocker, in 10 patients with severe left ventricular dysfunction. Simultaneous hemodynamic and radionuclide angiographic measurements were obtained at incremental doses of esmolol (2, 4, 8, 12 and 16 mg/min). At a dose of 4 mg/min, esmolol produced beats blockade: a decrease in heart rate from 91 +/- 4 to 83 +/- 4 beats/min (p less than 0.05) (mean +/- SEM) and a decrease in systolic aortic pressure from 133 +/- 5 to 128 +/- 5 mm Hg (p less than 0.05). At the maximal dose, the heart rate decreased to 79 +/- 3 beats/min (p less than 0.05) and biventricular function was depressed; the left ventricular ejection fraction decreased from 27 +/- 2 to 21 +/- 2% (p less than 0.05) and the right ventricular ejection fraction decreased from 38 +/- 2 to 29 +/- 2% (p less than 0.05). These changes were accompanied by increases in left ventricular end-diastolic volume (p less than 0.05), left ventricular end-systolic volume (p less than 0.05) and pulmonary artery wedge pressure (p less than 0.05), as well as a decrease in cardiac output (p less than 0.05). The hemodynamic abnormalities (which showed considerable interindividual variability) returned to near baseline levels 10 to 30 minutes after infusion was stopped. Thus, esmolol can be administered to patients with severe left ventricular dysfunction. The beneficial effect (beta-adrenergic blockade) is usually achieved with small doses without clinically important hemodynamic changes. At larger doses, however, significant changes in biventricular function may be observed.

Adrenergic beta-Antagonists↗
PubMed1997

Relation between contractile reserve and positron emission tomographic patterns of perfusion and glucose utilization in chronic ischemic left ventricular dysfunction: implications for identification of myocardial viability.

OBJECTIVES: This study sought to determine the incidence and extent of dobutamine-induced contractile reserve in myocardial regions characterized by classical and new positron emission tomographic (PET) patterns in patients with chronic ischemic left ventricular dysfunction. BACKGROUND: PET is considered the most accurate method for assessment of myocardial viability, which is traditionally identified by perfusion-metabolism mismatch. METHODS: In 23 patients, segmental wall thickening expressed by four echocardiographic scores at rest and during low dose (5 and 10 microg/kg body weight per min) dobutamine infusion and regional myocardial uptake of potassium-38 and fluorine-18 fluorodeoxyglucose (F-18 FDG) during glucose clamp were compared in 16 corresponding segments. RESULTS: Of a total of 368 segments, data analysis focused on 214 (58%) dyssynergic segments at baseline. Contractile reserve was identified with increasing incidence according to the six following PET patterns: 1) diminished perfusion and moderate reduction of F-18 FDG uptake (3 [11%] of 28 segments); 2) proportional reduction of perfusion and F-18 FDG uptake (10 [23%] of 43 segments); 3) perfusion-metabolism mismatch (19 [46%] of 41 segments); 4) preserved perfusion but moderate reduction of F-18 FDG uptake (13 [46%] of 27 segments); 5) preserved perfusion and F-18 FDG uptake (37 [59%] of 63 segments) compared with our normal database; and 6) normal perfusion but absolute increased F-18 FDG uptake (8 [73%] of 11 segments). In the latter category, only 7 of 24 segments had normal rest function. In dyssynergic segments with F-18 FDG uptake > or = 50% supplied by vessels with > or = 75% stenosis, improvement in contractility during dobutamine correlated with the presence of collateral channels. CONCLUSIONS: Myocardial regions with the traditional mismatch pattern of viability show contractile reserve in slightly < 50%. In segments with moderate reduction of F-18 FDG uptake, the contractile response to dobutamine is linked to the level of rest perfusion. Most segments with preserved perfusion and increased F-18 FDG uptake have impaired rest function, but contractile reserve is still present. These data suggest that in chronic ischemic left ventricular dysfunction, myocardial hibernation is a heterogeneous condition.

Dobutamine↗
PubMed1989

Baroreceptor, not left ventricular, dysfunction is the cause of hemodialysis hypotension.

Many patients with chronic renal failure experience profound hypotension during hemodialysis. This has been attributed both to autonomic and ventricular dysfunction. In an attempt to distinguish which, if either, is important in this role, we assessed both autonomic and left ventricular function in 10 such patients. Cardioactive medication was stopped 24 hours prior to the investigations. Autonomic function was assessed from day/night blood pressure and heart rate variation and from the hemodynamic response to tilting and the Valsalva maneuver using an intra-arterial ambulatory monitoring technique. Left ventricular function was assessed scintigraphically both before and during hemodialysis. Day/night variation was significantly reduced in the patients with chronic renal failure (BP 13/7 +/- 8/6 mmHg, HR 5 +/- 4) compared with a control population (BP 36/28 +/- 10/5 mmHg, HR 19 +/- 6). Nine patients had a "square wave" response to the Valsalva maneuver. Both of these abnormalities are usually seen in patients with heart failure and are attributed to volume overload and a consequent failure of baroreceptor response. Blood pressure fell during hemodialysis (mean fall 40/22 +/- 20/10 mmHg) in all patients, but heart rate did not change (-2 +/- 16) despite the hypotension. All patients had a normal or high resting ejection fraction (mean 66%, range 55-79%), and there was no change during dialysis. This indicates that the hypotension was not due to left ventricular dysfunction in this group of patients, but to a failure of the baroreceptor response to volume depletion during hemodialysis.

Adult↗
PubMed1991

[The long-term results of aortocoronary bypass surgery in patients with a severe preoperative left ventricular dysfunction].

We analyze retrospectively the short- and long-term results of coronary artery bypass surgery in 50 patients with severe left ventricular dysfunction operated in a period of 11 years. Sixty-six percent of patients had unstable angina and 12% of total presented angina post-acute postmyocardial infarction. Thirty-eight percent of patients were in preoperative functional class III-IV of NYHA. Three-vessel disease was present in 70% of the patients, two-vessel in 30%, and the main trunk was affected in 12% of the global. Hospital mortality was 4% (2/50) due to low cardiac output syndrome. Follow-up was available in all the survivors and ranged 6 months-11 years (mean: 4.8 +/- 3.1). During follow-up, 13 patients died, but in only six was due to cardiac cause. The 35 patients followed were in functional class I-II of NYHA. Eighty-eight percent of the patients were angina free at follow-up. Actuarial analysis, after exclusion of 3 patients who died of causes no directly related to the heart, showed an intrahospital survival rates of 96%; at first year was 92, at 3rd was 78%, and 5th year survival rates were 75%. In conclusion, patients with symptomatic angina and preoperative severe left ventricular dysfunction, coronary artery bypass graft has a low hospital mortality, is effective in improving angina and heart failure, and the long-term survival is acceptable.

Actuarial Analysis↗
PubMed1995

Relation between thallium uptake and contractile response to dobutamine. Implications regarding myocardial viability in patients with chronic coronary artery disease and left ventricular dysfunction.

BACKGROUND: Both thallium scintigraphy and dobutamine echocardiography have been used to assess myocardial viability. However, thallium uptake and the inotropic response to dobutamine are expressions of different cellular phenomena. The present study was undertaken to investigate the relation between the two methods in patients with chronic coronary artery disease and left ventricular dysfunction to derive insights into the mechanisms related to myocyte viability. METHODS AND RESULTS: Thirty patients (28 men and 2 women; age, 59 +/- 10 years) with chronic coronary artery disease and impaired left ventricular systolic function at rest (mean ejection fraction, 32 +/- 9%) were included in the study. Patients underwent transesophageal echocardiography during incremental doses of dobutamine from 2.5 to a maximum of 40 micrograms.kg-1.min-1 and single photon emission computed tomographic thallium scintigraphy using a stress-redistribution-reinjection protocol. The left ventricle was divided into 16 segments for analysis of echocardiographic and thallium images. Segmental myocardial contractile function was graded as normal, hypokinesis, akinesis, or dyskinesis at each incremental dose of dobutamine. Thallium uptake in each myocardial segment was graded on a 5-point scale from 0 (absent) to 2 (normal) for each of the stress, redistribution, and reinjection images. A segment was considered viable if the assigned thallium score was 1 or higher (normal uptake or only mild to moderate defect) in any of the stress, redistribution, or reinjection images. Among 472 myocardial segments available for analysis, 311 had resting wall motion abnormalities, of which 56% (173/311) showed contractile improvement with dobutamine (usually first observed at < or = 10 micrograms.kg-1.min-1) and 84% (262/311) were considered viable by thallium scintigraphy (P < .0001). Of the 262 segments considered viable by thallium, 167 (64%) had a contractile improvement with dobutamine; in contrast, only 6 of the 49 segments (12%) considered nonviable by thallium had a positive dobutamine response (P < .0001). Furthermore, a positive inotropic response to dobutamine was significantly related to the magnitude of thallium uptake: the proportion of segments with a positive dobutamine response rose with increasing magnitude of thallium uptake (P < .001). The disagreement between the two tests was related primarily to segments considered viable by thallium that did not show contractile improvement with dobutamine. CONCLUSIONS: These findings demonstrate the existence of a relation between thallium uptake and the inotropic response to dobutamine in patients with chronic coronary artery disease and left ventricular dysfunction. However, the proportion of segments showing a positive response to dobutamine is significantly lower than those with thallium uptake, suggesting that the cellular mechanisms responsible for a positive inotropic response to adrenergic stimulation require a higher degree of myocyte functional integrity than those responsible for thallium uptake.

Coronary Disease↗
PubMed1996

[Reversible severe ventricular dysfunction in female patient with eclampsia and HELLP syndrome].

A 23 year-old primigravid woman presented eclampsia and HELLP syndrome (hemolysis, elevated liver enzymes, low platelets) with severe left ventricular dysfunction after having a cesarean section. In a few weeks, clinic disappeared and ventricular function normalized. The importance of differential diagnosis between ventricular dysfunction in eclampsia and peripartum myocardiopathy is discussed.

Adult↗
PubMed1997

Combination neurohormonal blockade with ACE inhibitors, angiotensin II antagonists and beta-blockers in patients with congestive heart failure: design of the Randomized Evaluation of Strategies for Left Ventricular Dysfunction (RESOLVD) Pilot Study.

BACKGROUND: The Randomized Evaluation of Strategies for Left Ventricular Dysfunction (RESOLVD) Pilot Study is a trial of combination neurohormonal blockade using an angiotensin II antagonist (candesartan), an angiotensin-converting enzyme inhibitor (enalapril) and a beta-blocker (metoprolol) in patients with congestive heart failure (CHF). OBJECTIVES: Primary objectives of stage I are to determine the efficacy (via the 6 min walk test) and safety of candesartan alone, and in combination with enalapril, versus enalapril alone. Secondary objectives are to determine the effect of the above combinations on neurohormones, ventricular function, quality of life and symptoms. Stage II objectives are similar, evaluating the effect of the addition of metoprolol or placebo to the above medication(s). DESIGN: Randomized, two-stage trial consisting of a three-way comparison (stage I), followed by a 3 x 2 partial factorial design (stage II). SETTING: Sixty out-patient clinics in five countries. PATIENTS: Patients with symptoms of CHF (New York Heart Association functional classes II to IV), ejection fraction less than 40% and 6 min walk distance of 500 m or less. INTERVENTIONS: In stage I, 770 patients are randomized to receive candesartan alone, enalapril alone, or candesartan plus enalapril. After five months (end of stage I), patients are assessed for eligibility to be randomized in stage II. Those who are not candidates for randomization to beta-blocker or placebo are followed on their stage I medications until the end of the study. In stage II, patients are randomized to receive metoprolol or placebo for a further six months in addition to their stage I medications. Endpoints are measured at baseline, end of stage I (week 20) and end of stage II (week 46). STUDY STATUS: The study has recently completed follow-up in both stages. The findings from this study will be used to design a large scale mortality study that will help further define the role of neurohormonal blockade in patients with CHF.

Adrenergic beta-Antagonists↗
PubMed1991

[The effect of nifedipine and diltiazem on left ventricular function in patients with stable angina pectoris and severe left ventricular dysfunction].

In a double blind crossover five-week trial with a randomized onset in 12 patients with normal blood pressure, stable angina pectoris and more severe left ventricular dysfunction (ejection fraction less than or equal to 40%) the effect of placebo nifedipine and diltiazem on left ventricular function and tolerance of exercise was compared. The investigation was done by means of echocardiography after a load with stimulation of the heart by an oesophageal electrode. As compared with placebo, only diltiazem retarded significantly the period before development of stenocardia on stimulation of the heart. There was no significant difference between nifedipine and diltiazem as regards the effect exerted on the ejection fraction and time which elapsed after stimulation before stenocardia developed. The authors observed an unequal response of patients to the administration of nifedipine and diltiazem (some patients had less favourable findings, although they were not subjectively aware of this deterioration). Therefore these drugs must be administered to patients with angina pectoris and more severe left ventricular dysfunction with care and only if other drugs (nitrates or angiotensin convertase inhibitors) do not eliminate ischaemia and pain.

Adult↗
PubMed1985

Effect of short and long term administration of amiodarone on ischaemia-induced left ventricular dysfunction. Implications for combined antianginal drug therapy.

To asses haemodynamic effects of short and long term amiodarone on ischaemia-induced left ventricular dysfunction and to compare them with those of glyceryl trinitrate (nitroglycerin), beta-blocking and calcium antagonist drugs, 19 patients with chronic ischaemic heart disease were studied. All patients underwent simultaneous right heart catheterisation and equilibrium radionuclide angiocardiography at rest and during symptom-limited supine bicycle exercise. After control measurements without antianginal therapy, 10 patients received 7.5 mg/kg amiodarone intravenously over 5 minutes (short term study) followed by oral administration of amiodarone for 3 weeks (long term study). The remaining 9 patients were studied following the randomised administration of glyceryl trinitrate (0.8 mg sublingually), metoprolol (0.15 mg/kg intravenously) and nifedipine (5 ng/kg/min). During exercise known to provoke angina pectoris without therapy (control study), amiodarone improved myocardial oxygen consumption by reducing heart rate and systolic blood pressure without the negative inotropic effects seen after acute beta-adrenoceptor blockade. Comparisons with the haemodynamic profiles of other antianginal drugs suggest that amiodarone may be most effective when combined with glyceryl trinitrate or nifedipine for the treatment of ischaemic left ventricular dysfunction.

Adult↗
PubMed1999

Detection of adenoviral genome in the myocardium of adult patients with idiopathic left ventricular dysfunction.

BACKGROUND: The use of molecular biological techniques has demonstrated the importance of enteroviral infection of the myocardium in the pathogenesis of myocarditis and dilated cardiomyopathy in adults and adenovirus and enterovirus infection in children. The aim of this study was to determine the frequency of adenoviral infection of the myocardium of adults with impaired left ventricular function of unknown origin. METHODS AND RESULTS: Nested polymerase chain reaction (nPCR) was used to determine the frequency of detection of adenoviral DNA and enteroviral RNA in myocardial tissue samples from 94 adult patients with idiopathic left ventricular dysfunction and 14 control patients. Histological and immunohistological analyses were performed to detect myocardial inflammation. Adenoviral genomic DNA was detected by nPCR in 12 of the 94 patients with left ventricular dysfunction (in each case, adenovirus type 2), whereas enteroviral RNA was detected in another 12 patients. All control samples were negative for both viruses. In all patients, active myocarditis was excluded according to the Dallas criteria. However, there was significantly decreased CD2, CD3, and CD45RO T lymphocyte counts in the adenovirus-positive group compared with the adenovirus-negative group (P<0.05), whereas no differences were associated with enterovirus infection. CONCLUSIONS: Although enteroviruses are an important causative agent in the pathogenesis of myocarditis and dilated cardiomyopathy, this study shows that adenovirus infection is also important in the pathogenesis of left ventricular failure in adults. However, the pathogenetic basis of disease associated with adenovirus infection may be different than that after infection with other agents, particularly with respect to activation of the host immune response.

Adenoviridae Infections↗
PubMed2002

Depressed inotropic response to increased preload in rabbit hearts with left-ventricular dysfunction induced by chronic myocardial infarction.

Chronic (8 weeks) coronary artery ligation caused marked left-ventricular dysfunction (LVD) in rabbits. The positive inotropic effect observed in vivo with intraventricular injection of saline in sham-operated (control) animals was reversed in rabbits with LVD. In vitro, a step increase in filling pressure from 10 to 15 cm H(2)O caused an immediate increase, followed by a slow increase, in left-ventricular peak systolic pressure (LVP(max)) and cardiac output (CO) over 5-7 min in sham-operated hearts. No significant slow positive inotropic effect was observed in hearts with LVD in response to a standard increase in filling pressure. Progressive increases in filling pressure increased (LVP(max)) and CO to a maximum value at 20 cm H(2)O in control hearts. In the LVD group, progressive increases in filling pressure caused a negative inotropic response and reduced CO. Hearts from the LVD group were significantly dilated compared with control hearts but no significant changes in myocardial compliance were observed in beating or quiescent hearts. These studies reveal an impaired inotropic response to increased ventricular filling in LVD rabbit hearts; this defect included the depression of the slow inotropic response to an increased end-diastolic volume. These changes appear not to be accompanied by altered passive mechanical properties.

Animals↗
PubMed2003

Is the use of cardiopulmonary bypass for multivessel coronary artery bypass surgery an independent predictor of operative mortality in patients with ischemic left ventricular dysfunction?

BACKGROUND: l Coronary artery bypass grafting for patients with ischemic left ventricular dysfunction (ILVD) remains superior to medical therapy in terms of long-term survival. Recently, off-pump coronary artery bypass surgery has been shown to be very promising in achieving functional improvements with favorable operative mortality in this challenging group of patients. The aim of this study was to assess the risk factors responsible for operative mortality in this group of patients. METHODS: The records of 305 consecutive ILVD patients, who underwent primary isolated coronary artery bypass grafting for multivessel disease at The National Heart and Lung Institute, Imperial College, University of London, between January 1999 and January 2002, were reviewed retrospectively. Patients were considered to have ILVD if they had a left ventricular ejection fraction of 0.30 or less on preoperative coronary angiography. One hundred six patients were operated on using the off-pump coronary artery bypass surgery technique, and 199 patients were operated on using the conventional coronary artery bypass grafting technique with cardiopulmonary bypass. RESU;TS: Seven (6.6%) patients died in the off-pump coronary artery bypass surgery group, whereas 28 (14.1%) patients died in the cardiopulmonary bypass group (p = 0.05). Univariate analysis of all the preoperative characteristics was performed to identify the potential predictors of mortality in the whole group of ILVD patients. Potential predictors of mortality included symptom status (stable/unstable), chronic obstructive airway disease, dyspnea grade III and IV on the New York Heart Association classification, intravenous nitrates, preoperative use of intraaortic balloon pump, ventricular tachycardia or ventricular fibrillation, body surface area less than 2, and cardiopulmonary bypass. Only ventricular tachycardia or ventricular fibrillation was proved to act as an independent predictor of operative mortality in this group of ILVD patients, with an odds ratio of 29.6 (95% confidence interval, 8.9 to 98). CONCLUSIONS: This study showed that using cardiopulmonary bypass for multivessel coronary artery bypass grafting in patients with ILVD was not proved to act as an independent predictor of operative mortality.

Aged↗
PubMed2003

Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction.

BACKGROUND: Aldosterone blockade reduces mortality and morbidity among patients with severe heart failure. We conducted a double-blind, placebo-controlled study evaluating the effect of eplerenone, a selective aldosterone blocker, on morbidity and mortality among patients with acute myocardial infarction complicated by left ventricular dysfunction and heart failure. METHODS: Patients were randomly assigned to eplerenone (25 mg per day initially, titrated to a maximum of 50 mg per day; 3319 patients) or placebo (3313 patients) [correction] in addition to optimal medical therapy. The study continued until 1012 deaths occurred. The primary end points were death from any cause and death from cardiovascular causes or hospitalization for heart failure, acute myocardial infarction, stroke, or ventricular arrhythmia. RESULTS: During a mean follow-up of 16 months, there were 478 deaths in the eplerenone group and 554 deaths in the placebo group (relative risk, 0.85; 95 percent confidence interval, 0.75 to 0.96; P=0.008). Of these deaths, 407 in the eplerenone group and 483 in the placebo group were attributed to cardiovascular causes (relative risk, 0.83; 95 percent confidence interval, 0.72 to 0.94; P=0.005). The rate of the other primary end point, death from cardiovascular causes or hospitalization for cardiovascular events, was reduced by eplerenone (relative risk, 0.87; 95 percent confidence interval, 0.79 to 0.95; P=0.002), as was the secondary end point of death from any cause or any hospitalization (relative risk, 0.92; 95 percent confidence interval, 0.86 to 0.98; P=0.02). There was also a reduction in the rate of sudden death from cardiac causes (relative risk, 0.79; 95 percent confidence interval, 0.64 to 0.97; P=0.03). The rate of serious hyperkalemia was 5.5 percent in the eplerenone group and 3.9 percent in the placebo group (P=0.002), whereas the rate of hypokalemia was 8.4 percent in the eplerenone group and 13.1 percent in the placebo group (P<0.001). CONCLUSIONS: The addition of eplerenone to optimal medical therapy reduces morbidity and mortality among patients with acute myocardial infarction complicated by left ventricular dysfunction and heart failure.

Aged↗
PubMed1995

The vicious circle of ischemic left ventricular dysfunction.

Myocardial ischemia tends to be self-propagating, and minor events such as plaque rupture can lead to the catastrophic sequelae of myocardial infarction and death. The biology of the endothelium and the cardiac myocyte is crucial to the development of these vicious circles. The abnormal responses of the endothelial cell in atherosclerosis tend to provoke and propagate ischemia, and because of the limited metabolic reserve of the myocyte, even short periods of ischemia can lead to left ventricular dysfunction and arrhythmias. This article examines the clinical implications of the disordered biology of the endothelial cell and the myocyte that is the basis for ischemic left ventricular dysfunction.

Coronary Vessels↗
PubMed1980

Rest and exercise hemodynamic effects of oral hydralazine in patients with coronary artery disease and left ventricular dysfunction.

To determine the hemodynamic effects of afterload reduction at rest and during upright exercise in patients with coronary artery disease and left ventricular dysfunction, 12 patients were studied before and after taking 50-75 mg of oral hydralazine every 6 hours for 48 hours. Oxygen consumption and heart rate were unchanged from control both at rest and during two work loads on a bicycle ergometer. Cardiac output was significantly increased at rest and during both workloads. The arteriovenous oxygen difference was significantly reduced at rest and during exercise. Pulmonary capillary wedge pressure was also significantly lower at rest and during exercise. Systemic vascular resistance was reduced at rest, and exercise-induced vasodilation was augmented by the administration of hydralazine. Left ventricular end-diastolic volume and ejection fraction assessed by radionuclide angiocardiography were not significantly changed at rest or during exercise after hydralazine. Seven of the 12 patients have maintained clinical improvement during a follow-up of 6-12 months. Hemodynamic improvement provided by oral hydralazine at rest is maintained during moderate exertion in patients with coronary artery disease and left ventricular dysfunction. In selected patients, chronic afterload reduction with oral hydralazine may result in increased cardiac reserve, decreased pulmonary congestion or decreased myocardial oxygen demands, thereby improving or abolishing resting or exertional dyspnea or angina.

Aged↗
PubMed2003

'Tako-Tsubo cardiomyopathy' associated with syndrome malin: reversible left ventricular dysfunction.

A 66-year-old man developed a fever and had a syncopal attack during treatment with imipramine and amantadine for depression and Parkinson's disease. His muscular enzyme levels were very high, so he was diagnosed with incomplete syndrome malin and given hydration therapy. The electrocardiogram recorded an ST segment elevation like acute myocardial infarction in most leads, and the echocardiogram revealed left ventricular dysfunction with severe hypokinesis to dyskinesis of the anterior and apical wall regions, and hyperkinesis of the basal wall. One month from onset, the left ventricular contractility had not changed despite normal coronary arteries. Thallium-201((201)Tl) myocardial scintigraphy showed a perfusion defect and there was no accumulation of iodine-123((123)I) metaiodobenzylguanidine (MIBG) in the entire apex of the heart. Left ventricular function returned to normal and repeat (201)Tl scintigraphy showed recovery by the 4th month. However, there was still an absence of cardiac MIBG uptake. There are a number of reports from Japan of a syndrome demonstrating such reversible left ventricular dysfunction, called 'tako-tsubo cardiomyopathy', but the present case is the first to be associated with syndrome malin. A coronary microvascular abnormality and cardiac sympathetic denervation probably both play an important role in tako-tsubo cardiomyopathy.

3-Iodobenzylguanidine↗
PubMed1985

[Echocardiography in chronic aortic insufficiency. Prediction of the reversibility of left ventricular dysfunction following surgical correction].

UNLABELLED: The long term outcome of patients undergoing aortic valve replacement (AVR) for chronic aortic regurgitation (AR) is mainly determined by the reversibility or permanence of left ventricular dysfunction. We analysed the echocardiogram of 49 patients before and after surgery to identify the patients whose left ventricular dysfunction regressed completely after AVR. The patients were divided into 2 groups according to the results of the last postoperative echocardiogram: Group I: 25 patients whose left ventricular dimensions and wall motion reverted to normal; Group II: 24 patients with dilated and/or hypokinetic left ventricles. The two groups of patients were comparable for sex (Group I: 19 men, 6 women; Group II: 20 men, 4 women), age (Group I: 50,8 years, Group II: 53,9 years) and length of postoperative follow-up (Group I: 32 months, Group II: 34 months). The following parameters were measured and compared: diastolic and systolic left ventricular dimensions, myocardial mass and ventricular wall motion. RESULTS: Patients in Group I had less left ventricular dilatation than those in Group II (+35% vs +60%, p less than 0,001) and left ventricular contraction was better (FE: 62% vs 45%, p less than 0,001; %FS: 35% vs 23%, p less than 0,001). This study establishes that patients with chronic AR and % delta Dd less than 60%, an EF greater than 50% or %FS greater than 25%, have about a 90% probability of normalisation of LV function after AVR. If one of the indices exceeds these threshold values, the probability of permanent LV dilatation and/or hypokinesia after AVR is also about 90%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗