Background —Coronary endothelial dysfunction is characterized by vasoconstrictive response to the endothelium-dependent vasodilator acetylcholine. Although endothelial dysfunction is considered an early phase of coronary atherosclerosis, there is a paucity of information regarding the outcome of these patients. Thus, this study was designed to evaluate the outcome of patients with mild coronary artery disease on the basis of their endothelial function. Methods and Results —Follow-up was obtained in 157 patients with mildly diseased coronary arteries who had undergone coronary vascular reactivity evaluation by graded administration of intracoronary acetylcholine, adenosine, and nitroglycerin and intracoronary ultrasound at the time of diagnostic study. Patients were divided on the basis of their response to acetylcholine into 3 groups: group 1 (n=83), patients with normal endothelial function; group 2 (n=32), patients with mild endothelial dysfunction; and group 3 (n=42), patients with severe endothelial dysfunction. Over an average 28-month follow-up (range, 11 to 52 months), none of the patients from group 1 or 2 had cardiac events. However, 6 (14%) with severe endothelial dysfunction had 10 cardiac events ( P <0.05 versus groups 1 and 2). Cardiac events included myocardial infarction, percutaneous or surgical coronary revascularization, and/or cardiac death. Conclusions —Severe endothelial dysfunction in the absence of obstructive coronary artery disease is associated with increased cardiac events. This study supports the concept that coronary endothelial dysfunction may play a role in the progression of coronary atherosclerosis.
Whereas both leaflets tethering is related to preoperative ischemic MR, both leaflets tethering but with predominant contribution from augmented and progressive PML tethering is related to recurrent/persistent ischemic/functional MR late after surgical annuloplasty.
BackgroundThe aim of the present study was to determine whether repeated 60°C sauna treatment improves cardiac arrhythmias in chronic heart failure (CHF) patients, because ventricular arrhythmias are an important therapeutic target in CHF. Methods and Results Thirty patients (59±3 years) with New York Heart Association functional class II or III CHF and at least 200 premature ventricular contractions (PVCs)/24 h assessed by 24-h Holter recordings were studied. They were randomized into sauna-treated (n=20) or non-treated (n=10) groups. The sauna-treated group underwent a 2-week program of a daily 60°C far infrared-ray dry sauna for 15 min, followed by 30 min bed rest with blankets, for 5 days per week. Patients in the non-treated group had bed rest in a temperature-controlled room (24°C) for 45 min. The total numbers of PVCs/24 h in the sauna-treated group decreased compared with the non-treated group [848±415 vs 3,097±1,033/24 h, p<0.01]. Heart rate variability (SDNN, standard deviation of normal-to-normal beat interval) increased [142±10 (n=16) vs 112±11 ms (n=8), p<0.05] and plasma brain natriuretic peptide concentrations decreased [229±54 vs 419±110 pg/ml, p<0.05] in the sauna-treated group compared with the non-treated group. Conclusion Repeated sauna treatment improves ventricular arrhythmias in patients with CHF. (Circ J 2004; 68: 1146 -1151
The current study demonstrates that hypertension with LVH is associated with both coronary vascular remodeling and attenuated endothelial and nonendothelial coronary flow reserve.
n patients with chronic heart failure (CHF), vascular resistance is increased through the activation of neurohumoral systems, such as the sympathetic nervous, renin-angiotensin and endothelin systems. 1 Vascular endothelial function, which is mainly represented by endothelium-dependent vasodilatory function through the production of vasodilators derived from the endothelium such as nitric oxide (NO), prostacyclin and endothelium-derived hyperpolarizing factors, is impaired in CHF and affects clinical symptoms. 2-5 Impaired vascular endothelial function leads to increased vascular tone and vascular remodeling, which reduces peripheral blood flow and oxygen delivery to the skeletal muscles, followed by progressive exercise intolerance and clinical symptoms. [2][3][4][5] Therapies that improve endothelial function, such as angiotensin-converting enzyme inhibitors and regular exercise, improve the clinical symptoms and prognosis in CHF. [6][7][8][9] We reported that sauna therapy at 60°C induces vasodilation of the systemic and pulmonary arteries and veins, reduces cardiac preload and afterload and improves hemodynamics, clinical symptoms and cardiac arrythmia in patients with CHF. [10][11][12] We also clarified that the beneficial effects of sauna therapy for CHF are caused by improved vascular endothelial function and the normalizing of the neurohormonal systems. 13 Furthermore, we showed that repeated sauna therapy improved the survival of cardiomyopathic hamsters with CHF. 14 Vascular endothelial dysfunction in CHF is mainly due to decreased NO production induced by decreased levels of endothelial NO synthase (eNOS) expression and increased oxidative stress. [15][16][17] We have already reported that repeated sauna therapy increased arterial eNOS protein and mRNA expressions from the normal levels in healthy hamsters. 18 However, it is important to determine whether repeated sauna therapy could increase eNOS expression downregulated by CHF. The present study aims to investigate whether repeated sauna therapy modulates eNOS expression and NO production in CHF. Methods AnimalsWe used male TO-2 cardiomyopathic hamsters (Bio Breeders, Fitchburg, MA, USA) as a model of clinical dilated cardiomyopathy. These animals develop CHF (characterized by symptoms such as general edema and pleural effusion) at around 30 weeks of age and die within a year. 19,20 Male Syrian golden hamsters (Japan SLC, Hamamatsu, Japan) served as normal controls. All animals Background Vascular endothelial dysfunction is involved in the pathophysiology of chronic heart failure (CHF). It has been reported that sauna therapy, which allows thermal vasodilation, improves vascular endothelial dysfunction in patients with CHF. The present study investigates the mechanisms through which sauna therapy improves endothelial dysfunction induced by CHF. Methods and ResultsNormal control and male TO-2 cardiomyopathic hamsters were used. Thirty-week-old TO-2 hamsters were treated daily with an experimental far infrared-ray dry sauna system for 15 min at 39°C f...
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