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您的检索式：作者名="Michael Shochat"
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| 1 | Preventive treatment of alveolar pulmonary edema of cardiogenic origin显示文摘Objective To evaluate the efficacy of preventive treatment (PT) on alveolar pulmonary edema (APE) of cardiogenic origin using a monitor based on principles of internal thoracic impedance (ITI) measurements.Methods We conducted blinded clinical trials on patients with ST-elevation myocardial infarction (STEMI) and monitored whether the condition would progress to APE. ITI was measured noninvasively by the Edema Guard Monitor (EGM, model RS-207) every 30 min. The measurement threshold for the diagnosis of APE was fixed at > 12% decrease in ITI from baseline as described in our methodology. The patients were divided into one group that received standard treatment after the appearance of clinical signs of APE without considering the prediction of APE by EGM devise (Group 1), and another group of asymptomatic patients in whom development of APE was predicted by using only EGM measurements (Group 2). The latter participants’PT consisted of furosemide, intravenous nitroglycerine and supplemental oxygen. Results One-hundred and fifty patients with acute STEMI were enrolled into this study. Group 1 included 100 patients (53% males, age 64.1 ±12.6 years). Treatment was started after the clinical appearance of overt signs of APE. Group 2 included 50 patients (54% males, age 65.2 ±11.9 years) who received PT based on EGMmeasurements. Group 2 had significantly fewer cases of APE (n = 4, 8%) than Group 1 (n = 100, 100%) (P > 0.001). While APE was lethal in six (6%) Group 1 patients, PT resulted in prompt resolution of APE in all four (8%) Group 2 patients. Conclusion ITI is a usefulmodality for early diagnosis and PT of pulmonary edema of cardiogenic origin. | Gideon Charach Michael Shochat Alexander Rabinovich Oded Ayzenberg Jacob George Lior Charach Pavel Rabinovich | 2012 | Journal of Geriatric Cardiology2012，9，4： | 3 |
| 2 | Seasonal changes in blood pressure:Cardiac and cerebrovascular morbidity and mortality显示文摘Cold is a seasonal and circadian risk factor for cardioand cerebrovascular morbidity and mortality. Colder temperatures have been associated with higher blood pressure(BP), based on studies which show that BP levels measured during the summer months are generally lower than those measured during the winter months. Residents in geographic areas which have greater seasonal temperature differences show greater fluctuation in BP. Surprisingly, atmospheric pressure, rainfall, and humidity were not related to BP levels. The increased sympathetic nervous activity due to cold, as evidenced by elevated BP and by plasma and urinary catecholamines, has been proposed as being the underlying etiology. Patients with heart failure may experience, in cold conditions, endothelial dysfunction and produce fewer endogenous vasodilators(e.g., nitric oxide, prostaglandins) and more endogenous vasoconstrictors(e.g., endothelin), thus increasing afterload. Arterial stiffness is also related to seasonal BP changes. Increased BP, arterial stiffness and endothelial dysfunction could predispose to increased coronary and cerebrovascular events. Improved protection against lower temperatures or increased doses of existing medications or the addition of newer medications could lead to a reduction in increased cardiovascular mortality in winter. Here, we briefly review findings from existing literature and provide an update on seasonal long-term variation in BP along with the related complications. | Gideon Charach Michael Shochat Ori Argov Moshe Weintraub Lior Charach Alexander Rabinovich Oded Ayzenberg Jacob George | 2013 | World Journal of Hypertension2013，3，1： | 0 |
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