Chronic renal failure may be accompanied by reversible sympathetic activation, which appears to be mediated by an afferent signal arising in the failing kidneys.

Acute hypotension is an important complication of hemodialysis, but the underlying mechanisms remain poorly understood. Because hemorrhage-induced hypovolemia can trigger a sudden decrease in sympathetic activity resulting in bradycardia and vasodilation, we hypothesized that hemodialysis-induced hypovolemia also can trigger the same type of vasodepressor reaction, which would exacerbate the volume-dependent fall in blood pressure. We therefore measured blood pressure, vascular resistance, and sympathetic nerve activity (intraneural microelectrodes) during sessions of maintenance hemodialysis in 7 patients with and 16 patients without a history of hemodialysis-induced hypotension. During hemodialysis, blood pressure at first remained unchanged as calf resistance increased in both hypotension-resistant (from 37±4 to 49±5 U, P < 0.05) and hypotension-prone (from 42±6 to 66±12 U, P < 0.05) patients; sympathetic activity increased comparably in the subset of patients in whom it could be measured. With continued hemodialysis, calf resistance and sympathetic activity increased further in the hypotension-resistant patients, but in the hypotensionprone patients the precipitous decrease in blood pressure was accompanied by decreases in sympathetic activity, vascular resistance, and heart rate as well as symptoms of vasodepressor syncope. On an interdialysis day, both groups of patients increased vascular resistance normally during unloading ofcardiopulmonary baroreceptors with lower body negative pressure and increased heart rate normally during unloading of arterial baroreceptors with infusion of nitroprusside. These findings indicate that in a group of hemodialysis patients without diabetes or other conditions known to impair autonomic reflexes, hemodialysis-induced hypotension is not caused by chronic uremic impairment in arterial or cardiopulmonary baroreflexes but rather by acute, paradoxical withdrawal of sympathetic vasoconstrictor drive producing vasodepressor syncope. (J. Clin.

Symptomatic hypotension is a common and disabling complication of hemodialysis treatments. The incidence of symptomatic hypotensive episodes is particularly high in patients who have normal or low blood pressure at the initiation of dialysis and in patients who have large interdialytic weight gains. The aim of this study was to determine whether cooling the dialysate temperature from 37 degrees C to 35 degrees C improved tolerance to dialysis in a group of 12 of these "problem" patients. A double-blinded protocol was performed in six hypotension-prone and six large weight gainers who were subjected to two identical hemodialyses except for the dialysate temperature of 37 degrees C or 35 degrees C. Changes in biochemical parameters and weight were comparable during the two maneuvers. Recumbent blood pressure declined significantly (P < 0.01) during 37 degrees C dialysis but not 35 degrees C dialysis; blood pressure was significantly lower at 1, 2, and 3 hours of 37 degrees C dialysis compared to 35 degrees C dialysis (P < 0.05). Further, both supine and upright blood pressure was significantly lower following 37 degrees C dialysis (P < 0.02). This lower blood pressure was present in both subgroups of patients. All 18 episodes of symptomatic hypotension noted during the study occurred during 37 degrees C dialysis. A significantly greater increase in peripheral vascular resistance (calf blood flow was measured directly by venous occlusion plethysmography) occurred upon exposure to the 35 degrees C dialysate in both subgroups of patients (P < 0.01); supine and upright post-dialysis plasma norepinephrine values were also significantly greater (P < 0.001) after 35 degrees dialysis.(ABSTRACT TRUNCATED AT 250 WORDS)

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Summary:Transthoracic echocardiography (7TE) has substantial limitations for the study of abnormalities of the coronary tree. Transesophageal echocardiography (TEE) allows a more complete examination of the coronary arteries, particularly the proximal segments. This report describes the use of TEE after cardiac catheterization in the clinical management of a patient with unstable angina. While angiography fist showed the giant aneurysm of the left circumflex coronary artery, TEE, by revealing an active thrombus of the lumen, prompted an immediate surgical resolution.Key words: coronary atery aneurysm, transesophageal echocardiography, thrombose, embolism, angiographic Case ReportAn 80-year-old man with ahistory of noninsulin-dependent diabetes inellitus presented to an outlying facility with 36 h of unstable angina and electrocardiographic (ECG) evidence of lateral ischemia. While his chest pain was relieved with nitrates and heparin, the ECG showed ongoing T-wave changes in the lateral leads. Cardiac isoenzymes confirmed a non-Q wave myocardial infarction, with a peak creatine phosphokinase of 3 18 IUA and a 16% MB fraction. The patient was stabilized with aspirin, nitrates, and beta blockers, and was discharged 9 days after his admission. Twice within 6 weeks, he wa$ readmitted to the same outlying facility for recurrent angina and lateral ECG changes and was finally transferred to our facility for cardiac catheterization. The left ventricular (LV) angiogram showed an ejection fraction of 35% with diffuse hypokinesis, an inferobasilar aneurysm, and akinesis of the septum. There was no visible thrombus. Triple-vessel coronary artery disease was identified. The right coronary artery was diffusely diseased and totally occluded in its midportion. The distal vessel filled retrograde from the left system. The left main coronary artery showed mild luminal irregularities with a distal tapering of about 30%. The left anterior descending coronary artery had a critical 95% stenosis at inid vessel and the distal vessel showed diffuse disease. There was a giant aneurysm of the proximal left circumflex artery from which two large obtuse marginals originated, providing TIM1 grade 11 flow to the posterolateral wall (Fig. I). No definite filling defect could be appreciated in the coronary aneurysm to explain its slow distal flow, and the patient continued to have an unstable anginal pattern despite maximum medical managcment. The low flow in the obtuse marginals led us to suspect recurrent coronary embolisms originating from the coronary aneurysm; TEE was performed to examine this possibility. The images clearly demonstrated a large thrombus involving most of the coronary aneurysm (Fig. 2). The giant aneurysm measured 4 X 5 cm and was located in the proximal left circumflex artery in close proximity to the left atrial appendage. Color-flow imaging demonstrated turbulent flow circumventing the large thrombus within the coronary aneurysm (Fig. 3). These findings concurred with our hypothesis that recurrent emboli from this giant...