Subject(s)
Arteriovenous Fistula , Embolization, Therapeutic , Hypertension, Portal , Humans , Hypertension, Portal/complications , Hypertension, Portal/diagnostic imaging , Mesenteric Artery, Superior/diagnostic imaging , Arteriovenous Fistula/complications , Arteriovenous Fistula/diagnostic imaging , Arteriovenous Fistula/therapy , Portal VeinABSTRACT
OBJECTIVE: Calcium channel blockers (CCBs) are used as antihypertensive agents and have a strong vasodilatory effect; however, the sympathetic activation mediated by baroreflex might cause adverse effects. A recently developed CCB, azelnidipine, decreases the heart rate (HR) while lowering blood pressure (BP), possibly by inhibiting sympathetic nerve activity in animal models. In this study, we evaluated whether azelnidipine inhibited sympathetic nerve activity, compared to amlodipine, in primary hypertensive patients. DESIGN AND METHODS: We conducted a prospective, randomized, open-label, and crossover study of 14 patients. We measured the patients' BP, HR and baroreflex sensitivity, and directly recorded muscle sympathetic nerve activity (MSNA), via microneurography, after treatment with either CCB for 8 weeks. RESULTS: Although systolic and diastolic BPs did not differ between the azelnidipine and amlodipine groups, the HR in the azelnidipine group significantly decreased compared with that in the amlodipine group. MSNA was significantly reduced in the azelnidipine compared with the amlodipine group (47.7â±â14.9 vs. 61.5â±â10.7â bursts per 100 beats, Pâ<â0.05). However, no significant difference was observed in terms of the baroreflex control of HR, or MSNA, between the two groups. CONCLUSION: Our data show, first, that azelnidipine, compared with amlodipine, exerted a favorable effect on sympathetic nerve activity, without affecting baroreflex sensitivity, in hypertensive patients. These results indicate that azelnidipine might be useful for treating hypertensive patients, in whom hypertension is complicated by heart failure and ischemic heart disease.
Subject(s)
Amlodipine/pharmacology , Antihypertensive Agents/pharmacology , Azetidinecarboxylic Acid/analogs & derivatives , Baroreflex/drug effects , Calcium Channel Blockers/pharmacology , Dihydropyridines/pharmacology , Hypertension/drug therapy , Sympathetic Nervous System/drug effects , Azetidinecarboxylic Acid/pharmacology , Baroreflex/physiology , Blood Pressure/drug effects , Blood Pressure/physiology , Cross-Over Studies , Essential Hypertension , Female , Heart Rate/physiology , Humans , Hypertension/physiopathology , Male , Middle Aged , Prospective StudiesABSTRACT
Activation of the sympathetic nervous system is augmented in patients with type 2 diabetes mellitus (DM). Pioglitazone, an anti-diabetic drug, improves insulin resistance, but its influence on sympathetic nerve activity is not clear. To identify the relationship between insulin resistance and sympathetic activity, we examined muscle sympathetic nerve activity (MSNA) in controlled type 2 DM patients with alpha-glucosidase inhibitor (GI). We measured MSNA and calculated homeostasis model assessment of insulin resistance index (HOMA-IR) in twelve DM patients treated with alpha-GI and thirteen age-matched healthy subjects. In DM patients with alpha-GI, all parameters were reexamined after three months of treatment with pioglitazone. MSNA and HOMA-IR were significantly greater in DM patients with alpha-GI compared to healthy subjects. Hemoglobin A1c did not differ in DM patients before and after pioglitazone. However, pioglitazone significantly decreased MSNA in DM patients compared with alpha-GI (21.7±5.2 vs. 32.0±6.8 burst/min, p<0.01). Furthermore, MSNA level in pioglitazone was similar to that in healthy subjects. HOMA-IR significantly decreased after pioglitazone, and a significant relationship was found between the absolute change in MSNA and HOMA-IR (r=0.65, p<0.05). These results suggest that improved insulin resistance with pioglitazone provides an additional effect on inhibition of sympathetic nerve activity.
Subject(s)
Diabetes Mellitus, Type 2/drug therapy , Diabetes Mellitus, Type 2/enzymology , Glycoside Hydrolase Inhibitors , Insulin Resistance/physiology , Sympathetic Fibers, Postganglionic/drug effects , Sympathetic Fibers, Postganglionic/enzymology , Thiazolidinediones/pharmacology , Action Potentials/drug effects , Action Potentials/physiology , Aged , Diabetes Mellitus, Type 2/physiopathology , Female , Humans , Hypoglycemic Agents/pharmacology , Hypoglycemic Agents/therapeutic use , Male , Middle Aged , Muscle, Skeletal/blood supply , Muscle, Skeletal/enzymology , Muscle, Skeletal/innervation , Pioglitazone , Sympathetic Fibers, Postganglionic/physiopathology , Thiazolidinediones/therapeutic use , alpha-Glucosidases/physiologyABSTRACT
Swallow syncope is a relatively rare syndrome that is treatable when diagnosed. A 66-year-old woman was referred to the department of cardiology because she had been suffering from recurrent syncopal attacks associated with swallowing. An ambulatory electrocardiogram revealed atrial and ventricular asystoles immediately after swallowing soup or tea that were reproducible (max. RR 3.5 s). An electrophysiological study did not detect sinus nodal or atrioventricular nodal dysfunction. The patient had no underlying esophageal disease or cardiac disorder. The patient's symptoms resolved after permanent pacemaker implantation. This report reviews the diagnosis, mechanism and management of swallow syncope.
