Marked Improvement In Cardiac Function Research Articles

Improvement of Cheyne-Stokes Respiration, Central Sleep Apnea and Congestive Heart Failure by Noninvasive Bilevel Positive Pressure and Medical Treatment

A 57-year-old man was admitted with dyspnea. Clinical evaluation revealed atrial fibrillation and congestive heart failure (CHF). Standard medical therapy of CHF failed to completely improve the dyspnea and polysomnography revealed Cheyne-Stokes respiration with central sleep apnea (CSR-CSA). He was equipped with noninvasive positive pressure ventilation (NPPV) with bilevel positive airway pressure (BiPAP). The combined therapy of medical treatment of the CHF and administration of NPPV with BiPAP reduced the CSR-CSA. This regimen resulted in marked improvement of cardiac function, evaluated by echocardiography, and reduction of plasma concentration of brain natriuretic peptide. After the patient recovered from CHF and was discharged from hospital, he continued to use NPPV with BiPAP at home. In patients with CHF, it is important to be aware of sleep-related breathing disorders because treatment will not only improve the hypoxemia, but also the cardiac dysfunction.

777 Exposure of spontaneous hypertensive rats to ambient particulate matter affects cardiovascular performance in a Langendorff model

A total of 32 patients, age range 27-83 years (mean 59±14 years), were admitted with acutely decompensated chronic heart failure (CHF; idiopathic, 62.5%; ischaemic, 36%; others, 1.5%). All patients were in NYHA functional class IV, with an EF of 7-35% (mean, 18±7%). Intravenous levosimendan was administered to all patients, loading dose, 3-12 μg/kg over 10 minutes (n=29), followed by a continuous infusion of 0.1-0.2 μg/kg/minute for 24 hours (n=32). Haemodynamic parameters of heart rate (HR) and blood pressure (BP) were measured prior to treatment and at 10 and 30 minutes, and 12 and 24 hours after commencement of therapy. Urine output and laboratory measurements were also made prior to and following levosimendan treatment. Adverse events, mortality rate, length of stay in hospital and readmission rates were also assessed. A slight reduction in BP was seen in patients following the initial loading dose of levosimendan, which quickly recovered and was maintained up to 24 hours (systolic BP, 95±18 mmHg at baseline vs 106±16 mmHg at 24 hours, p<0.05). HR significantly decreased following levosimendan treatment compared to baseline (93±16 vs 81±10 bpm; p<0.001). A significant diuresis was observed at 24 and 48 hours following treatment compared with baseline (57±29 vs 130±52 mL/hour, and 57±29 vs 120±42 mL/hour, respectively; both p<0.0001). A marked improvement in cardiac function was observed from NYHA functional class IV at baseline to NYHA class II-III following levosimendan treatment (p<0.0001). No significant changes in laboratory measurements were evident 24 hours after treatment or at discharge. Furthermore, no serious levosimendan-associated adverse events were measured. A significant reduction in the average length of hospital stay was seen in patients treated with levosimendan compared to previous hospital admissions where levosimendan was not given; 12±5 days without levosimendan compared with 5±1.5 days with levosimendan (p<0.0001). The mean number of hospital re-admissions at 180 days due to CHF was also reduced following levosimendan compared with before treatment (0.5±1.0 vs 2.0±1.5, respectively; p<0.0001). In addition to demonstrating immediate clinical and haemodynamic benefits in patients with severe heart failure, levosimendan may offer a longterm clinicaland cost-benefit for the management of this patient population.

Enhanced endogenous adenosine production and protection of the heart after transplantation.

Inhibition of adenosine metabolism and supply of nucleotide precursors resulted in marked improvement in cardiac function and increase in cardiac ATP concentration following cardioplegic arrest and hypothermic ischemia. Stimulation of endogenous adenosine production could be thus an effective treatment following cardiac transplantation.

Evidence for calcitonin gene-related peptide-mediated ischemic preconditioning in the rat heart

Previous studies have suggested that calcitonin gene-related peptide (CGRP) may play an important role in the mediation of ischemic preconditioning. In the present study, we examined the release of CGRP during ischemic preconditioning and the effect of preconditioning frequency on this effect in the isolated rat heart. Thirty minutes of global ischemia and 40 min of reperfusion caused a significant cardiac dysfunction and an increase in the release of creatine kinase (CK) during reperfusion. Preconditioning with one, two or three cycles of 5-min ischemia and 5-min reperfusion caused a marked improvement of cardiac function and a decrease in the release of CK, and there was no difference in the degree of improvement among groups. The protective effects of ischemic preconditioning were abolished by the CGRP receptor antagonist CGRP 8-37. A single preconditioning cycle induced a significant increase in the release of CGRP in the coronary effluent. In the hearts treated with two or three preconditioning cycles, the level of CGRP was highest in the first cycle, and was gradually decreased with increasing number of cycles of preconditioning. These results suggest that the protective effects of ischemic preconditioning are mediated by endogenous CGRP in the isolated rat heart.

A Case of Insulin Dependent Diabetes Mellitus with Marked Improvement of Cardiac Function after Live Donor Renal Transplantation

A Case of Insulin Dependent Diabetes Mellitus with Marked Improvement of Cardiac Function after Live Donor Renal Transplantation

The Effects of Pulmonary Infection on Cardiorespiratory Functions in Chronic Emphysema.

Investigations of cardiorespiratory functions in pulmonary diseases have in recent years contributed much to the understanding of the development of pulmonary heart disease. Harvey et al.’ in a recent publication have stressed the importance of anoxia in patients with chronic pulmonary emphysema as a cause for the deterioration of heart function. According to them, acute anoxia may precipitate the development of congestive heart failure and the relief of anoxia may bring about marked improvement in cardiac function. The main causes of acute anoxia may be bronchial obstruction and acute pulmonary infection. Two cases of emphysema were recently observed in which the development of acute pulmonary infection and anoxia was associated with congestive heart failure. Recovery from the infection and anoxia was accompanied by regression of the signs of congestive heart failure. In one case, also, the interesting effects of treatment with adrenocorticotropic hormone on pulmonary functions in the different stages of pulmonary emphysema were recorded.