Angiotensin AT1 receptor inhibition. Effects on hypertrophic remodeling and ACE expression in rats with pressure-overload hypertrophy due to ascending aortic stenosis.

BACKGROUND: We tested the hypothesis that long-term administration of the specific angiotensin II subtype 1 (AT1)-receptor blocker BMS-186295 will regress hypertrophy and modify left ventricular angiotensin converting enzyme (ACE) expression in rats with ascending aortic stenosis. METHODS AND RESULTS: Six weeks after surgery, rats with ascending aortic stenosis were randomized to receive either the AT1-receptor blocker BMS-186295 50 mg.kg-1.d-1 (n = 49), amlodipine 2.5 mg.kg-1.d-1 (n = 48) as a positive control for systemic vasodilation, or no drug (n = 48) and compared with sham-operated rats (n = 39). Drug treatment was continued for 15 weeks. Left ventricular ACE mRNA levels were measured by ribonuclease protection assay. The left ventricular/body weight ratio was increased 43% in hearts from rats with untreated left ventricular hypertrophy (LVH) versus control hearts (P < .05). However, there was no difference in either the left ventricular/body weight ratio (2.78 +/- 0.08 versus 2.81 +/- 0.20 mg/g; P = NS) or myocyte cross-sectional area in the AT1-blocker-treated versus untreated LVH hearts. Amlodipine also showed no effect on regression of hypertrophy. In vivo left ventricular systolic pressure was significantly higher in untreated LVH versus sham-operated rats (193 +/- 8 versus 118 +/- 4 mm Hg; P < .05), and there was a similar severe elevation of left ventricular systolic pressure in the AT1-blocker- and amlodipine-treated LVH groups (189 +/- 9 and 188 +/- 16 mm Hg; P = NS versus untreated LVH). In vivo left ventricular end-diastolic pressure was higher in the untreated LVH than in the sham-operated rats (14.8 +/- 2.3 versus 7.0 +/- 0.5 mm Hg; P < .05). Left ventricular end-diastolic pressure was lower in the AT1-blocker-treated (11.0 +/- 1.7 mm Hg) and amlodipine-treated rats (11.5 +/- 1.8 mm Hg) and was similar to left ventricular end-diastolic pressure in the sham-operated rats (P = NS). Left ventricular ACE mRNA levels were elevated in untreated LVH rats but were normalized in both the AT1-blocker-treated rats and amlodipine-treated rats. CONCLUSIONS: Long-term AT1-receptor blockade did not regress LVH in rats with persistent systolic pressure overload due to ascending aortic stenosis. However, both AT1-receptor blockade and amlodipine improved in vivo left ventricular end-diastolic pressure in association with the normalization of left ventricular ACE mRNA levels.

Stent jail: a minimum-security prison.

Small but significant side branches (particularly those with baseline ostial narrowing) may be further compromised by stent placement within parent vessel segments. Despite the theoretical risks associated with dilating branches in stent jail, the procedure was successfully completed in 84%, with minimal complications (mostly balloon rupture and local dissection) and no cases of balloon entrapment or deterioration of the final result achieved in the parent vessel.

Disseminated herpesvirus infection during pregnancy.

A case of disseminated herpes simplex virus infection during pregnancy is reported, and 26 similar cases are reviewed. The present case was unusual in that it occurred in the 12th week of gestation, whereas all but one of the other cases occurred in the second or third trimester. This rare complication is generally preceded by a flu-like prodrome with or without oral or genital lesions. The clinical presentation is (1) encephalitis without hepatic involvement, (2) hepatitis with or without central nervous system findings, or (3) disseminated skin lesions. When the liver is involved, rapidly progressive hepatic necrosis and severe coagulopathy are common and the mortality is high. Early diagnosis and early institution of antiviral chemotherapy with acyclovir greatly improve the outcome for both mother and infant.

Doppler echocardiographic assessment of the St. Jude Medical prosthetic valve in the aortic position using the continuity equation.

To test whether the continuity equation can be applied to the noninvasive assessment of prosthetic aortic valve function, Doppler echocardiography was performed in 67 patients (mean age, 58 +/- 14 years) within 10 +/- 6 days after valve replacement with St. Jude Medical valves. All patients were clinically stable and without evidence of valve dysfunction. Valve size ranged from 19 to 31 mm, and ejection fraction ranged from 30% to 75%. With the parasternal long-axis view, the left ventricular outflow diameter measured just proximal to the prosthetic valve correlated well with valve size (r = 0.92). Doppler-derived maximal gradients ranged from 9 to 71 mm Hg. Effective prosthetic aortic valve area by the continuity equation ranged between 0.73 cm2 for a 19-mm valve and 4.23 cm2 for a 31-mm valve. With analysis of variance, effective orifice area differentiated various valve sizes (p less than 10(-14)) better than did gradients alone (p = 0.003) and correlated better with actual valve orifice area (r = 0.83 versus - 0.40). A Doppler velocity index, the ratio of peak velocity in the left ventricular outflow to that of the aortic jet, averaged 0.41 +/- 0.09 and was less dependent on valve size (r = 0.43). Thus, the continuity equation can be applied to the assessment of prosthetic St. Jude valves in the aortic position. By accounting for flow through the valve, it provides an improved assessment over the sole use of gradients in the evaluation of prosthetic valve function.