Short atrioventricular delay reduces the degree of mitral regurgitation in patients with a sequential dual-chamber pacemaker

This study was performed in a population of sequential dual-chamber pacemaker-patients with isolated mitral regurgitation (MR) to identify the "ideal atrioventricular (AV) delay" and to determine the effect of sequential pacing with the ideal AV delay on MR degree. Twenty consecutive patients (age 69 +/- 7 years; 45% men) hospitalized at our institution for symptomatic III degree AV block and isolated MR were studied. All received a dual-chamber pacemaker programmed in DDD at a rate of 70 pulses/minute. The ideal AV delay was selected using echo-color Doppler parameters; it was defined as that resulting in a lower degree of MR and in the highest cardiac output. The mean "optimal short" AV delay resulted in 98 +/- 7 ms. At short AV delay we observed a significant reduction in MR severity (regurgitant fraction from 48 +/- 12% to 25 +/- 10% and jet area from 15 +/- 2 to 9 +/- 2 cm2; p <0.0001) together with an increase in stroke volume (68 +/- 16 vs 88 +/- 15 ml; p = 0.007) and mitral early-to-late peak velocity ratio (0.79 +/- 0.33 vs 1.38 +/- 0.37; p <0.0001). In conclusion, a short AV delay may be used to improve cardiac output in sequential paced patients with pure, isolated M

Short-term results of transdermal estrogen replacement therapy in cardiovascular disease-free postmenopausal females with and without hypertension

BACKGROUND: Many studies have shown that estrogen replacement with oral micronized 17 beta-estradiol reduces the risk of cardiovascular disease. The aim of the present study was to evaluate the efficacy of transdermal estrogen replacement therapy in improving the risk profile of cardiovascular disease in postmenopausal women. METHODS: Two hundred and fifty postmenopausal women were enrolled from the "Bene Essere Donna" Center and grouped according to the absence (Group I, n = 175; mean age 54.6 +/- 3.5) or presence of mild to moderate hypertension (Group II, n = 75; mean age 54.1 +/- 4.5). Total cholesterol, HDL cholesterol, LDL cholesterol, triglycerides, glucose and fibrinogen levels were tested in all women. The total study population was treated with estrogen replacement therapy for 12 months: hysterectomized women received 17 beta-estradiol (0.05 mg/die), while non-hysterectomized women received 17 beta-estradiol 0.05 mg/die plus 5 mg/die of medroxyprogesterone acetate for 12 days during every 28-day cycle. After 12 months, blood pressure and blood chemistry were measured as baseline. RESULTS: Total cholesterol, LDL cholesterol and glucose levels decreased in both groups. HDL cholesterol levels increased significantly only in the sub-group of Group II treated with estrogen plus progesterone. Triglycerides glucose and fibrinogen blood levels decreased in both groups. No cardiovascular events were recorded during the first year of follow-up. CONCLUSION: Transdermal estrogen replacement therapy should be considered as a therapeutic support in order to contrast the elevated cardiovascular risk in postmenopausal wome

Changes in serum levels of N-terminal procollagen type III propeptide as an index of postinfarction ventricular remodeling

The levels of aminoterminal propeptide of type III procollagen (PIIINP) can be used as an index of collagen breakdown. The aim of our study was to evaluate modifications in serum concentration of PIIINP (PIIINPs) in patients with a first episode of myocardial infarction. We examined 70 patients admitted at our Institution for acute myocardial infarction and 10 normal subjects. PIIINPs dosage was obtained by radioimmunoassay method utilizing a commercial available kit. All patients underwent three PIIINPs dosages: within 24 hours after admission, at 6 and 12 months after myocardial infarction. Control values were 0.4 +/- 0.1 U/ml. In 38 patients (Group I) PIIINPs levels increased at 6 and 12 months after infarction: 0.53 +/- 0.2, 0.75 +/- 0.2 and finally 0.76 +/- 0.1 U/ml. In the remaining 32 patients (Group II) PIIINPs values increased at 6 months and then returned to baseline at 12 months: 0.56 +/- 0.2, 0.75 +/- 0.1 and then 0.46 +/- 0.1 U/ml. The end-diastolic volume index did not change significantly in Group I (from 93.7 +/- 21 to 79.7 +/- 20 ml/m2) while it decreased after 12 months in Group II (from 88.9 +/- 13 to 58.6 +/- 11 ml/m2; confidence interval 95% from 2 to 55 ml/m2; p = 0.03). Similarly, there was no significant variation in end-systolic volume index (ESVI, from 39.7 +/- 11 to 36.9 +/- 11 ml/m2) and ejection fraction (from 60 +/- 10 to 59 +/- 15%) in Group I; while in Group II ESVI decreased significantly (from 33.6 +/- 13 to 20 +/- 5 ml/m2, confidence interval 95% from 3 to 24 ml/m2; p = 0.02) and ejection fraction improved (from 62 +/- 11 to 72 +/- 15%; confidence interval 95% from -20 to -1%; p = 0.04). In conclusion, patients with elevated levels of PIIINPs at 12 months did not improve ventricular function while patients with PIIINPs returning to baseline at 12 months had an improvement. Our results suggest an active participation of newly formed collagen in post-infarct ventricular remodeling. Therefore PIIINPs may be a marker of this process