Background-Prior studies suggest that the causes of calcific aortic valve (AV) disease involve chronic inflammation, lipoprotein levels, and calcium metabolism, all of which may differ among race-ethnic groups. We sought to determine whether AV thickness differs by race-ethnicity in a large multi-ethnic population-based cohort.
While recent guidelines for the treatment of acute heart failure syndromes (AHFS) recommend pharmacotherapy with vasodilators in patients without excessively low blood pressure (BP), few reports have compared the relative efficiency of vasodilators on hemodynamics in AHFS patients. The present study aimed to assess the differences in hemodynamic responses between intravenous carperitide and nicorandil in patients with AHFS. Thirty-eight consecutive patients were assigned to receive 48-h continuous infusion of carperitide (n = 19; 0.0125-0.05 μg/kg/min) or nicorandil (n = 19; 0.05-0.2 mg/kg/h). Hemodynamic parameters were estimated at baseline, and 2, 24, and 48 h after drug administration using echocardiography. After 48 h of infusion, systolic BP was significantly more decreased in the carperitide group compared with that in the nicorandil group (22.1 ± 20.0 % vs 5.3 ± 10.4 %, P = 0.003). While both carperitide and nicorandil significantly improved hemodynamic parameters, improvement of estimated pulmonary capillary wedge pressure was greater in the carperitide group (38.2 ± 14.5 % vs 26.5 ± 18.3 %, P = 0.036), and improvement of estimated cardiac output was superior in the nicorandil group (52.1 ± 33.5 % vs 11.4 ± 36.9 %, P = 0.001). Urine output for 48 h was greater in the carperitide group, but not to a statistically significant degree (4203 ± 1542 vs 3627 ± 1074 ml, P = 0.189). Carperitide and nicorandil were differentially effective in improving hemodynamics in AHFS patients. This knowledge may enable physicians in emergency wards to treat and manage patients with AHFS more effectively and safely.
Ivabradine increases stroke volume, but does not have a negative impact on blood pressure (BP). Thus, a patient with low BP can benefit from treatment with ivabradine. A 72-year-old Japanese woman with asthma and chronic bronchitis presented with dyspnea. Her heart rate (HR) was 126 beats per minute and an electrocardiogram showed sinus tachycardia. The chest X-ray showed cardiomegaly and pulmonary congestion. A transthoracic echocardiogram (TTE) showed reduced left ventricular ejection function (LVEF) and severe functional mitral regurgitation (MR). We diagnosed her with inappropriate sinus tachycardia (IST) and heart failure (HF) due to tachycardia-induced cardiomyopathy. After resolving the pulmonary congestion with diuretics, we administered a minimum dose of bisoprolol, which resulted in re-exacerbation of the HF. Because IST was persistent, we initiated treatment with ivabradine. As soon as ivabradine was started, the HR decreased, the BP gradually increased, and HF compensation was achieved. Bisoprolol was continued and losartan was started. In summary, we used ivabradine for a patient with tachycardia, low BP, a low LVEF, and severe MR. By optimizing the medical therapy, exercise tolerance improved and she was discharged. The serum brain natriuretic peptide was significantly reduced and TTE showed an improved LVEF and reduced MR.
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We managed a patient who had low blood pressure (BP) due to tachycardia, reduced left ventricular ejection function (LVEF), and severe mitral regulation (MR). In this case, ivabradine had a novel effect; specifically, heart rate was reduced and BP increased. As a result of the drug effects, we could prescribe a renin-angiotensin-system inhibitor. With optimal medical therapy, LVEF was restored and functional MR was reduced. In similar cases, ivabradine can be a key drug for medical therapy of heart failure.>
The patient was a 67-year-old female diagnosed with dilated cardiomyopathy. She had chronic atrial fibrillation (AF) with bradycardia and low left ventricular function (left ventricular ejection fraction (LVEF) 40%). She was admitted for congestive heart failure. She remained New York Heart Association (NYHA) functional class III due to AF bradycardia. Pacemaker implantation was necessary for treatment of heart failure and administration of dose intensive -blockers. As she had normal His-Purkinje activation, we examined the optimal pacing sites. Hemodynamics of His-bundle pacing and biventricular pacing were compared. Pulmonary capillary wedge pressure (PCWP) was significantly lower on Hisbundle pacing than right ventricular (RV) apical pacing and biventricular pacing (13 mmHg, 19 mmHg, and 19 mmHg, respectively) with an almost equal cardiac index. Based on the examination we implanted a permanent pacemaker for Direct His-bundle pacing (DHBP). After the DHBP implantation, the LVEF immediately improved from 40% to 55%, and BNP level decreased from 422 pg/ml to 42 pg/ml. The number of premature ventricular complex (PVC) was decreased, and non sustained ventricular tachycardia (NSVT) disappeared. Pacing threshold for His-bundle pacing has remained at the same level. His-bundle pacing has been maintained during 27 months and her long-term DHBP can improve cardiac function and the NYHA functional class. (J Arrhythmia 2006; 22: 245-250)
The initial use of carperitide therapy safely reduces PCWP in ADHF patients with LVSD and baseline systolic BP may be useful for predicting the response to initial carperitide therapy for ADHF with LVSD.
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