Disrupted regulation of ghrelin production under antihypertensive treatment in spontaneously hypertensive rats.

BACKGROUND: Ghrelin is an acylated peptide hormone mainly secreted from the stomach. When administrated externally it modulates vascular tone mainly through the regulation of autonomic nerve activity. However, the effects of blood pressure (BP) on the production and secretion of ghrelin remain to be clarified. METHODS AND RESULTS: We examined the stomach and plasma levels of ghrelin in spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats after a 4-week-intervention with antihypertensive agents (candesartan-cilexetil [ARB], doxazosin [DZN], metoprolol [MP], reserpine [RES]) to clarify the influence of BP on the secretion of ghrelin. The effect of these agents on ghrelin production and secretion were examined by comparing vehicle-treated controls (WKY-Intact, SHR-Intact). Treatment with the 4 antihypertensive drugs all yielded a significant decline in systolic BP in both SHR and WKY. Under these conditions, significantly lower levels of stomach and plasma ghrelin were detected in WKY treated with ARB (P<0.05), DZN (P<0.05), MP (P<0.05) and RES (P<0.05) compared with WKY-Intact, whereas no significant change in the ghrelin levels in the stomach and plasma were detected in SHR under the same treatments. CONCLUSIONS: The findings imply that the production and secretion of ghrelin are controlled by the ambient vascular tone and vice versa in normotensive WKY. This inter-relationship between ghrelin and BP seems to be disrupted in SHR.

Predictor of underlying myocardial damage in normally functioning left ventricle with narrow QRS complex: relationship between QRS duration at right ventricle pacing and iodine-123 metaiodobenzylguanidine myocardial scintigraphy.

OBJECTIVE: Washout rate of iodine-123 metaiodobenzylguanidine (MIBG) myocardial scintigraphy is correlated with the degree of myocardial damage. The aim of this study is to ascertain whether there is any relationship between QRS complex duration at right ventricle (RV) pacing and the degree of myocardial damage assessed by I-123 MIBG myocardial scintigraphy in normally functioning left ventricle. METHODS: The study included 22 patients (10 men and 12 women, ranging in age from 48 to 89 years), with atrioventricular (AV) block (n = 15) and sick sinus syndrome (n = 7). All patients had baseline QRS duration of less than 120 ms and received implantation of a DDD-mode permanent pacemaker. Iodine-123 MIBG myocardial scintigraphy was performed before the pacemaker implantation, and QRS duration at RV pacing at a rate of 70 ppm was calculated immediately after the implantation. RESULTS: With the use of RV pacing, QRS duration was prolonged ranging from 122.4 to 185.6 ms with a mean of 153.2 +/- 15.2 ms. Washout rate of I-123 MIBG myocardial scintigraphy (WR) was calculated as ranging from 5.0 to 83.0% with a mean of 44.2 +/- 17.5%. There was a strong correlation between WR and QRS duration at RV pacing (r = 0.735, p < 0.001). CONCLUSIONS: It was confirmed that WR of I-123 MIBG was correlated positively with QRS duration at RV pacing. Measurement of QRS duration may be helpful to evaluate the degree of underlying myocardial damage even in the normally functioning left ventricle.

Discrepancy between Doppler and catheter measurements of pressure gradients across small-size prosthetic valve.

OBJECTIVES: The exact role of pressure gradient across the prosthetic valve estimated from Doppler flow velocity remains controversial. This in-vivo study was designed to assess the actual discrepancy between Doppler and catheter measurements of the pressure gradients for small bileaflet prosthetic valves in the aortic position. METHODS: Bileaflet prosthetic valves (19 mm-ATS) were implanted into the aortic position in pigs, and pressure gradients across the valves were examined by volume loading under right heart bypass. The pressure gradient obtained by catheter was defined as the conventional peak-to-peak gradient between the left ventricle and aorta. The peak Doppler gradients were calculated from the maximal instantaneous Doppler velocity with the ultrasound probe positioned on the diaphragm at the level of the cardiac apex. RESULTS: There were strong correlations between pressure gradients and cardiac output. The Doppler gradient was constantly higher than the catheter values, and the resultant discrepancy between Doppler and catheter measurements was directly dependent on cardiac output (y=9.9x+0.6, r2=0.55). For cardiac output > or = 5.0 L/min, the difference between Doppler and catheter gradients reached 40 mmHg, and maximum differences of up to 80 mmHg were observed. CONCLUSIONS: In view of the presence of striking overestimation of catheter gradient by Doppler measurement, Doppler ultrasound should be used cautiously to assess small-size bileaflet prosthetic valve function with consideration of the patient's hemodynamic state.

Recurrent pericardial tamponade from atrial hemangioma.

We encountered a 72-year-old woman with a left atrial hemangioma arising in the appendage and growing like an extracardiac mass. Life-threatening cardiac tamponade, recurrent over a 5-year clinical course, was the only sign of this rare tumor. The extraatrial growth pattern of the tumor made it difficult to distinguish the cardiac origin from a paracardiac mass. With the aid of cardiopulmonary bypass, the tumor was removed from the left atrium at the base of the appendage. Pathologic diagnosis was a combination of cavernous- and venous-type hemangioma. The postoperative course was uneventful, and the patient was doing well with no pericardial effusion at the 10-month follow-up.

C-reactive protein and atrial fibrillation. Is inflammation a consequence or a cause of atrial fibrillation?

To clarify whether inflammation is a cause or consequence of atrial fibrillation (AF), we measured high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-alpha) before and after pharmacological cardioversion in 15 patients with paroxysmal AF. Levels of hs-CRP, IL-6, and TNF-alpha after cardioversion were significantly higher than those in controls (P < 0.05). Furthermore, the levels of these indices did not differ significantly even at 24 hours and 2 weeks after cardioversion. These results suggest that inflammation is a causative agent of paroxymal AF.