Utility of brain natriuretic peptide to predict right ventricular dysfunction and clinical outcome in patients with acute pulmonary embolism.
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OBJECTIVE(S): To investigate the hemodynamic effects and safety of R 80122, a novel selective phosphodiesterase (PDE) III inhibitor, and its solvent hydroxypropyl-beta-cyclodextrin. DESIGN: Prospective, randomized study. SETTING: Operating theater of a university hospital in the Netherlands. PARTICIPANTS: Twelve patients with impaired left ventricular function scheduled for coronary artery bypass grafting after induction of anesthesia were included. INTERVENTIONS: R 80122 (n = 6) or its solvent (n = 6) was administered using the same infusion regimen. A bolus of 0.1 mL/kg (= 0.1 mg/kg R 80122) was infused over 10 minutes followed by a maintenance infusion of 5 microliters/kg/min (5 micrograms/kg/min R 80122) over 20 minutes. MEASUREMENTS AND MAIN RESULTS: Compared with the solvent, patients receiving R 80122 did not show any significant changes in heart rate, arterial blood pressure, or pulmonary artery pressures. However, R 80122 produced a marked increase (P < 0.05) in cardiac output (thermodilution) and echocardiographically obtained percentage area reduction. No arrhythmias or ischemic episodes occurred during the infusion period. The plasma half-life of R 80122 was 10.6 +/- 1.9 minutes. CONCLUSIONS: R 80122 appears to be a potent positive inotropic agent in these patients. Its use is not associated with marked vasodilation, it is devoid of positive chronotropic effects, and it can be administered safely in patients with impaired left ventricular function.
A 59-year-old male was admitted to the emergency department because of sustained chest oppression. Electrocardiography revealed J type ST depression and peaked T wave in leads II, III, aVF, and V4-V6. No stenosis was found in the coronary arteries by urgent coronary angiography. Left ventricular abnormal wall movement with akinesis in the base and hyperkinesis in the apical area was observed and improved on the 12th day. Myocardial scintigraphy with iodine-123-metaiodobenzylguanidine showed completely defective images and decreased accumulation in the base with combined thallium-201 and iodine-123-beta-methyl-p-iodophenyl-pentadecanoic acid. Myocardial biopsy on the 12th day disclosed contraction band necrosis. The diagnosis was catecholamine-induced cardiomyopathy caused by pheochromocytoma.
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Mitral regurgitation (MR) is a frequent complication of end-stage cardiomyopathy. Historically, these patients were managed either medically or with mitral valve replacement, both associated with poor outcomes. We studied 125 patients with cardiomyopathy and severe MR who were managed with mitral reconstruction. One hundred twenty-five patients with 4+ MR, left ventricular ejection fractions from 8% to 24% (mean 14%), and New York Heart Association class III or IV symptoms were prospectively studied. All patients underwent mitral valve repair with an undersized flexible annuloplasty ring. There was one intraoperative death and five 30-day mortalities. Intraoperative echocardiography showed mild to trivial MR in seven patients, and no residual MR in the majority of patients. There were 26 late deaths; three of these patients had progression of the disease and underwent transplantation. One- and 2-year actuarial survival has been 80% and 70%, respectively. New York Heart Association class has improved for all the patients from a preoperative mean of 3.2 +/- 0.2 to 1.8 +/- 0.4 postoperatively. At 24-month follow-up, all patients showed an improvement of ejection fraction, cardiac output, and end-diastolic volumes, along with a reduction in sphericity index and regurgitant volume. Mitral valve repair with an undersized flexible annuloplasty ring is a safe and effective approach to correct MR in cardiomyopathy patients. All observed changes contribute to reverse remodeling and the restoration of the normal left ventricular geometric relationship. Mitral reconstruction offers a new treatment strategy for patients with MR and end-stage heart failure.
An 84-yr-old man with previous anterior wall myocardial infarction presented with shortness of breath and palpitations. His symptoms were attributed to myocardial ischemia, and he was referred for a stress 99mTc-sestamibi SPECT imaging study with gating. The images showed minimal left ventricular ischemia, but a dilated and hypokinetic right ventricle suggested pulmonary pathology as the probable etiology of his presenting symptoms. A subsequent ventilation perfusion study was consistent with the diagnosis of multiple pulmonary emboli. Thus, 99mTc-sestamibi SPECT imaging with gating provides information about right ventricular perfusion and function, enhancing the clinical utility of stress myocardial perfusion imaging.
The effect of PTCA on global and regional left ventricular systolic function, isovolumic relaxation, chamber and muscle stiffness were studied in 30 patients with angina pectoris, previous non-Q wave anterior myocardial infarction (AMI) and significant stenosis of the left anterior descending coronary artery (LAD). In 11 of the 30 patients the condition was stable, but it was unstable in 19. Left ventricular angiograms were obtained before and 4.85 +/- 3.67 months after PTCA. The RAO was in the 30 degree projection, with the silhouette of the left ventricle sliced into 90 regions; changes in left ventricular volume, pressure and anterior wall thickness during the full cardiac cycle, together with dp/dt were demonstrated. After PTCA, global ejection fraction increased from 68.77 +/- 5.96% to 76.57 +/- 3.18%, P < 0.001. Impaired contractility was found in 29/90 (32.2%) regions before PTCA and in 5/90 (5.6%) after PTCA, P < 0.001. The time constant of the isovolumic pressure fall decreased after PTCA (52.56 +/- 17.40 ms vs 39.61 +/- 11.26 ms, P < 0.01). Elastic chamber stiffness coefficient decreased (0.022 +/- 0.003 vs 0.008 +/- 0.004, P < 0.001) and peak rate of left ventricular filling increased (319.0 +/- 107.9 ml.min-1 vs 396.8 +/- 201.4 ml.min-1, P < 0.05) after PTCA. The muscle stiffness coefficient was within normal values before and did not change after PTCA. The study findings show that in patients with persistent angina pectoris after non-Q wave AMI, complex systolic and diastolic ischaemic dysfunction occurs. This dysfunction can be reversed after successful PTCA of LAD.
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