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PubMedDate not supplied

Effect of intravenous fructose-1,6-diphosphate on myocardial contractility in patients with left ventricular dysfunction.

STUDY OBJECTIVE: To examine the effects of fructose-1,6-diphosphate on myocardial performance using nuclear scintigraphy. DESIGN: Prospective, randomized, single-blind, parallel study. SETTING: Urban teaching hospital clinical research center. PATIENTS: Individuals with New York Heart Association functional class II-III heart failure (mild to moderate). INTERVENTIONS: Subjects received either intravenous fructose-1,6-diphosphate 125 mg/kg or normal saline 1.3 ml/kg every 12 hours over 10 minutes for four consecutive doses. Left ventricular performance was assessed by radionuclide ventriculography at baseline and within 60 minutes after the fourth infusion. Vital signs were monitored throughout the study period. MEASUREMENTS AND MAIN RESULTS: Fructose-1,6-diphosphate resulted in a modest 7% increase in left ventricular ejection fraction (p < 0.05). Peak ejection rate and peak diastolic filling rate did not change significantly. There were no changes in blood pressure or heart rate with either fructose-1,6-diphosphate or placebo. CONCLUSIONS: Fructose-1,6-diphosphate produces a modest but significant increase in left ventricular ejection fraction in patients with mild to moderate heart failure.

Adult↗
PubMed1997

Severe ventricular dysfunction secondary to subarachnoid hemorrhage.

A 39-year-old man was brought to the emergency department in a coma. The electrocardiogram showed partial left bundle-branch block and ST elevation in precordial leads, and serum creatinine kinase activity was elevated. Two-dimensional echocardiography revealed severe biventricular dysfunction. Autopsy demonstrated the presence of subarachnoid hemorrhage. Coronary arteries and the myocardium were macroscopically normal.

Adult↗
PubMedDate not supplied

Transient left ventricular dysfunction in childhood sickle cell disease.

For unclear reasons, myocardial infarction is rare in childhood sickle cell disease, whereas lung, bone, and brain infarcts are more common. During vasoocclusive crisis and infection, acute myocardial ischemia and chronic volume overload from anemia may result in myocardial dysfunction. We report a child who had reversible cardiac dysfunction that mimicked myocardial infarction.

Child↗
PubMed2001

Alterations in myocardial creatinine kinase (CK) and lactate dehydrogenase (LDH) isoenzyme-distribution in a model of left ventricular dysfunction.

The purpose of the current study was to evaluate myocardial creatinine kinase (CK) and lactate dehydrogenase (LDH) systems in a model of epinephrine-induced cardiomyopathy in rabbits. Eight rabbits received four repetitive epinephrine infusions (300 mg/kg/60 min, i.v.) in 12-day intervals and eight untreated rabbits served as controls (CTRL). Echocardiography demonstrated a significant deterioration of LV function as well as increased LV-diameter and -mass index in catecholamine-induced cardiomyopathy. Histological examination revealed that repetitive catecholamine infusion resulted in LV fibrous areas with collagenous content and an increase in myocyte width (16.9+/-0.8 microm vs. CTRL 12.9+/-0.9; P<0.05). LV dysfunction was associated with a decreased total LV lactate dehydrogenase activity (LDH; 0.43+/-0.03 IU/mg protein vs. CTRL 0.52+/-0.04; P<0.05) whereas total creatinine kinase activity was unchanged (CK; 7.30+/-0.63 IU/mg protein vs. CTRL 9.20+/-0.49, n.s.). Furthermore, myocardial LDH isoenzymes were shifted with a decrease in LDH(1) and an increase in LDH2 and LDH3 (LDH(1): 84.90+/-2.60% vs. CTRL 94.50+/-0.40; LDH2: 7.30+/-1.20% vs. 1.50+/-0.13; LDH3: 5.40+/-0.90% vs. 3.20+/-0.25; all P<0.05). Foetal B-CK isoenzymes were significantly increased (CK-MB 5.30+/-0.66 vs. 2.20+/-0.35%; P<0.05). The current study demonstrates changes in cardiac energy metabolism including an impaired LDH activity with a shift towards anaerobic isoenzymes as well as a more efficient CK system in a model of catecholamine-induced LV dysfunction.

Animals↗
PubMed2004

[Neurohormonal prediction of post-infarction ventricular dysfunction and coronary disease].

Little information is available about the potential role of brain (type B) natriuretic peptide in patients with acute myocardial infarction. We therefore analyzed peptide levels, measured at discharge from our coronary care unit, in 56 patients admitted with a diagnosis of acute myocardial infarction. We examined peptide concentrations in the light of different features in our patients, and found a significant association between natriuretic peptide levels and the two most important prognostic factors: left ventricular ejection fraction, and the severity and extent of coronary disease. Type B natriuretic peptide was a good predictor of these features, and we conclude that concentration of type B natriuretic peptide, measured at discharge from the coronary care unit, provides important clinical and prognostic information in patients with acute myocardial infarction.

Coronary Disease↗
PubMed2001

CAPRICORN: a story of alpha allocation and beta-blockers in left ventricular dysfunction post-MI.

Beta-blocker therapy is beneficial both after myocardial infarction and in mild, moderate and severe chronic heart failure. Recent sub-group analysis of the Goteborg Metoprolol Trial and the AIRE study confirm that patients receiving beta-blockers in the setting of post-MI heart failure fare better than patients not receiving this therapy. For all these reasons the CAPRICORN trial of carvedilol in post-MI LV dysfunction was an important and eagerly awaited trial. The results were presented for the first time at The American College of Cardiology on March 20 2001. CAPRICORN randomised 984 patients to placebo and 975 to carvedilol between 3 and 21 days (mean 10) after a confirmed MI. Patients had to have evidence of a left ventricular ejection fraction 40% or less. All patients had received ACEI therapy for at least 48 hours prior to randomisation. The mean ejection fraction of the patients recruited was 32.7% in the placebo group and 32.9% in the carvedilol group. Follow-up was for a mean of 15 months (maximum 2.7 years). All cause mortality was 15.3% (151 deaths) in the placebo group and 11.9% (116 deaths) in the carvedilol group, giving a hazard ratio of 0.77 (0.60-0.98) and a significance of p = 0.031. And yet this agent will probably not be given a licence for this indication in the European Union and the USA. The reason is one of trial design and statistical declarations. Some way into the trial the Steering Committee decided to change the primary end-point form all-cause mortality to two co-primary end-points and to allocate their alpha power of 0.05 unevenly between the combined end-points of all cause mortality and cardiovascular hospitalisation (alpha 0.045) and all cause mortality (alpha 0.005). In the end neither was achieved, one because of the large number of non-specific hospitalisations for chest pain and the mortality effect because it was allocated a punitive and unachievable target of p < 0.005. The trial is thus officially neutral despite showing convincing clinical benefit. Clearly arcane matters of statistical plans do matter and steering committees should think very carefully before changing the primary end-points of major trials.

Adrenergic beta-Antagonists↗
PubMed1994

Coronary artery bypass grafting for left ventricular dysfunction.

In patients with severe coronary disease and poor left ventricular function, coronary artery bypass grafting has a positive impact on long-term survival. In presence of angina or documented ischemia, it is beneficial in protecting functioning muscle against future infarction. In patients with heart failure and no angina, it is a rational option when large areas of akinetic but viable myocardium are identified preoperatively; under these circumstances, recovery of myocardial function is the goal of coronary revascularization. Obviously, reliable methods of assessing myocardial viability and contractile reserve are required for an accurate selection of patients. Advances in perioperative management, including myocardial preservation, have consistently reduced the operative risk in the most recent series, and more appropriate selection criteria have substantially contributed to the improved long-term survival. Variables associated with higher hospital mortality as well as factors influencing long-term outcome have been identified. The beneficial effect of coronary artery bypass grafting on the functional status of patients has been documented in several studies, and the improvement in left ventricular function has been objectively demonstrated. The concepts and the data presented in this review may help to define the present role of coronary artery bypass grafting in the treatment of ischemic cardiomyopathy.

Angina Pectoris↗
PubMed1987

Preoperative left ventricular dysfunction and operative risks in coronary bypass surgery.

Preoperative left ventricular function variables were evaluated as potential risk factors for peroperative and postoperative complications in 183 consecutive patients undergoing coronary bypass surgery. Fifty-six patients had no abnormal criteria and 127 had at least one criterion (AN). The incidence of history of infarction was significantly greater in the AN (71.6 percent) than in the N (39.6 percent) group (p less than 0.04). During the early postoperative course, N and AN differentiated significantly in (1) the need for inotropic therapy (II vs 30 percent, p less than 0.05); (2) intra-aortic balloon pump (0 vs 13 percent); (3) arrhythmias (20 and 40 percent, p less than 0.002); and (4) stay in the Intensive Care Unit (2.3 +/- 0.8 and 3.9 +/- 2 days, p less than 0.01). Perioperative necrosis and mortality were not different. During a follow-up period of two years, N and AN did not show any difference in mortality and recurrence of angina.

Arrhythmias, Cardiac↗
PubMed1994

[Long survival (an average of 7 years) after coronary bypass in patients with severe left ventricular dysfunction].

The inclusion criteria of this study were a left ventricular ejection fraction of less than 40% with global left ventricular hypokinesis; left ventricular aneurysms and valvular lesions were excluded. From January 1970 to December 1990, 155 patients fulfilling these criteria had Class III or IV angina and 49 patients had Class II or III dyspnoea. The average left ventricular ejection fraction was 31 +/- 7%. Over this 20 year period two surgical techniques were used: Group I (79 patients operated between 1970 and 1981) myocardial revascularisation with intermittent aortic clamping by an internal mammary artery pedicle on the left anterior descending artery and simple venous bypass grafts; Group II (76 patients operated between 1982 and 1990) myocardial revascularisation under oxygenated cardioplegia by internal mammary artery pedicle on the left anterior descending artery associated with sequential venous bypass grafts. The average number of bypass grafts was 1.6 in Group I and 3.7 in Group II (p = 0.001). The early postoperative mortality (first month) was 5.2% it was lower in Group II (2.6%) than in Group I (7.6%) (p = 0.01). After 79 +/- 14 months follow-up, 6 patients were lost to follow-up, 51 patients had died secondarily and there were 90 survivors. Globally, 80% of deaths were of cardiac origin, 38% from cardiac failure. The actuarial 5, 10 and 15 year survival rates were 79 +/- 7%, 63 +/- 10% and 36 +/- 15% respectively. The 5 year survival in Group I was 71 +/- 10% compared with 88 +/- 8% in Group II (p = 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗