ABSTRACT
<p><b>BACKGROUND</b>Atrial fibrillation (AF) is the most frequent tachyarrhythmia in patients with a permanent pacemaker. Angiotensin II receptor antagonists have a protective effect against the occurrence of AF in patients with heart diseases. This study aimed to assess the effectiveness of olmesartan in the prevention of new-onset AF and AF burden in atrioventricular block (AVB) patients with dual-chamber (DDD) pacemaker implantation.</p><p><b>METHODS</b>This was a single-center, prospective, randomized, single-blind, controlled clinical study. A total of 116 AVB patients, who received DDD pacemakers implantation with the percentage of ventricular pacing (VP%) ≥40% from April 22, 2011 to December 24, 2012, were prospectively randomized to olmesartan group (20 mg per day; n = 57) or control group (n = 59). Patients were followed up using pacemaker programming, 12-lead electrocardiography in the intrinsic sinus rhythm, laboratory examinations, and transthoracic echocardiography at 24 months. Atrial high rate events (AHREs) were defined as 180 beats/min over a minimum of 5 min. AF burden was calculated by the number of hours with AHREs divided by the number of measurement hours.</p><p><b>RESULTS</b>Ten (17.5%) patients in the olmesartan group and 24 patients (40.7%) in the control group occurred new-onset AF, and the difference between two groups was statistically significant (P = 0.04). AF burden was lower in olmesartan group than that in control group (8.02 ± 3.10% vs. 13.66 ± 6.14%, P = 0.04). There were no significant differences in mean days to the first occurrence of AHREs and mean cumulative numbers of AHREs between two groups (P = 0.89 and P = 0.42, respectively). Moreover, olmesartan group had smaller values of maximal P-wave durations and P-wave dispersion (PD) after 24 months follow-up compared with the control group (109.5 ± 7.4 ms vs. 113.4 ± 7.1 ms, P = 0.00; and 40.6 ± 4.5 ms vs. 43.3 ± 4.4 ms, P = 0.02, respectively). Left ventricular end-diastolic diameter and left ventricular ejection fraction were not significantly different between two groups (both P > 0.05).</p><p><b>CONCLUSION</b>This study suggested that 24-month of olmesartan therapy could reduce new-onset AF and AF burden in patients with DDD pacemakers.</p><p><b>CLINICAL TRIAL REGISTRATION</b>ChiCTR-TRC-12004443; http://www.chictrdb.org.</p>
Subject(s)
Aged , Female , Humans , Male , Middle Aged , Angiotensin Receptor Antagonists , Therapeutic Uses , Atrial Fibrillation , Drug Therapy , Atrioventricular Block , Drug Therapy , Imidazoles , Therapeutic Uses , Single-Blind Method , Tetrazoles , Therapeutic UsesABSTRACT
<p><b>BACKGROUND</b>Coronary endothelial shear stress (ESS) triggered the development of atherosclerosis. However, the effect of calcium channel antagonist on the distribution of ESS remained unclear.</p><p><b>METHODS</b>Twenty consecutive patients with acute coronary syndrome (ACS) 48 hours after maximal medication with single left anterior descending artery stenosis < 50% were studied. Nicardipine was intravenously injected at 1 µg/kg after a bolus of 10 mg in order to achieve mean blood pressure (MBP) reduced by 10% or more, or the heart rate increased by 10 - 15 beats/min. Hemodynamic variables and angiogram at baseline and during injection of nicardipine were recorded, respectively. Coronary artery 3-D reconstruction was used for the analysis of ESS.</p><p><b>RESULTS</b>Distal reference-vessel-diameter and minimal lumen diameter decreased significantly from (2.42 ± 0.41) mm and (1.47 ± 0.49) mm at baseline to (2.22 ± 0.35) mm and (1.35 ± 0.49) mm at maximal drug-dosage (P = 0.018 and 0.020, respectively). Nicardipine did not change blood velocity. Lowest mean shear stress at segments 2-mm distal to plaque increased significantly from (0.034 ± 0.519) Pa at baseline to (0.603 ± 0.728) Pa (P = 0.013) at peak effect of drug.</p><p><b>CONCLUSIONS</b>Nicardipine was associated with the constriction of diseased vessel segment that adapted to the reduction of blood pressure, without dynamic change of blood velocity at each stage of whole cardiac cycle. Increased ESS value at segments distal to plaque reflected the cardioprotection by nicardipine (ChiCTR-TRC-10000964).</p>
Subject(s)
Aged , Female , Humans , Male , Middle Aged , Acute Coronary Syndrome , Angina, Unstable , Diagnostic Imaging , Drug Therapy , Blood Pressure , Coronary Angiography , Coronary Vessels , Heart Rate , Hemodynamics , Nicardipine , Therapeutic UsesABSTRACT
<p><b>BACKGROUND</b>The definitive treatment for myocardial ischemia is reperfusion. However, reperfusion injury has the potential to cause additional reversible and irreversible damage to the myocardium. One likely candidate for a cardioprotection is adenosine. The present study aimed at investigating the effect of intravenous adenosine on clinical outcomes in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI).</p><p><b>METHODS</b>Patients with STEMI within 12 hours from the onset of symptoms were randomized by 1:1:1 ratio to receive either adenosine 50 µg×kg(-1)×min(-1) (low-dose group, n = 31), or 70 µg×kg(-1)×min(-1) (high-dose group, n = 32), or saline 1 ml/min (control group, n = 27) for three hours. Drugs were given to the patients immediately after the guide wire crossed the culprit lesion. Recurrence of no-reflow, TIMI flow grade (TFG) and TIMI myocardial perfusion grade (TMPG), and collateral circulation were recorded. The postoperative and preoperative ST segment elevation sum of 18-lead electrocardiogram (ECG) and their ratio (STsum-post/STsum-pre) were recorded, as well as the peak time and peak value of CK-MB enzyme. Serial cardiac echo and myocardial perfusion imaging were performed at 24 hours and 6 months post-stenting. The primary endpoint was left ventricular function, and infarct size. The secondary end-point was the occurrence of cardiac and non-cardiac death, non-fatal myocardial infarction, and heart failure.</p><p><b>RESULTS</b>A total of 90 STEMI patients were studied. No-reflow immediately after stent procedure was seen in 11 (35.5%) patients in the control group, significantly different from 6.3% in the low-dose group or 3.7% in the high-dose group (both P = 0.001). STsum-post/STsum-pre in the low-dose and high-dose groups was significantly different from the control group (low-dose group vs. control group, P = 0.003 and high-dose group vs. control group, P = 0.001), without a dose-dependent pattern (P = 0.238). The peak value of CK-MB enzyme was significantly reduced in the high-dose group compared to the control group (P = 0.024). Compared to the left ventricular ejection fraction (LVEF) in control group, LVEF in the low-dose group increased by 5.8% at 24 hours (P = 0.012) and by 10.9% at 6 months (P = 0.007), LVEF in the high-dose group increased by 9.5% at 24 hours (P = 0.001) and by 10.0% at 6 months (P = 0.001), respectively. Significant reduction of infarct size by 24.2% was detected in the high-dose group vs. low-dose or control groups (P = 0.008). There was no significant difference regarding secondary endpoints at 6 months among the treated groups. Cardiac function by NYHA classification in both the low-dose and the high-dose groups was improved significantly (P = 0.013, P = 0.016).</p><p><b>CONCLUSION</b>Intravenous adenosine administration might significantly reduce the recurrence of no-reflow, with resultant improved left ventricular systolic function. High-dose adenosine was further associated with significant reduction of infarct size.</p>
Subject(s)
Aged , Female , Humans , Male , Middle Aged , Adenosine , Therapeutic Uses , Angioplasty, Balloon, Coronary , Echocardiography , Myocardial Infarction , Drug Therapy , Therapeutics , Ventricular Function, LeftABSTRACT
<p><b>BACKGROUND</b>Fluid dynamic mechanisms attributed to coronary bifurcation lesions remain a subject of study. The present study aimed at investigating the hemodynamic change of wall shear stress (WSS) in patients with coronary bifurcation lesions treated by double kissing (DK) crush or one-stent with final kissing balloon inflation (FKBI).</p><p><b>METHODS</b>Eighty-one patients with bifurcation lesions treated by stenting who had 3-D model reconstruction were studied. The bifurcation vessels were divided into main vessel (MV), main branch (MB), side branch (SB), and polygon of confluence (POC). MB and SB were classified by internal- and lateral-subsegments, respectively.</p><p><b>RESULTS</b>The baseline magnitude of WSS in proximal MV, POC-MV, POC-MB, POC-SB and MB-internal segments increased significantly, compared to MB-lateral, SB-internal and SB-lateral. DK crush had the potential of uniformly reducing WSS, turbulent index and the WSS gradient. The WSS value at the POC-SB and SB in the one-stent group remained higher. The turbulent index and WSS gradient between the POC-SB minus the SB-lateral had equal predictive values for in-stent restenosis (ISR).</p><p><b>CONCLUSION</b>Fluid dynamic results favor the use of DK crush over the one-stent technique.</p>
Subject(s)
Aged , Female , Humans , Male , Middle Aged , Angioplasty, Balloon, Coronary , Coronary Artery Disease , Therapeutics , Hemodynamics , PhysiologyABSTRACT
<p><b>BACKGROUND</b>Hypertrophic obstructive cardiomyopathy (HOCM) carries an increased risk for sudden cardiac death. No data regarding the percutaneous transseptal myocardial ablation (PTSMA) and epicardial left ventricular pacing (LVP) were reported.</p><p><b>METHODS</b>Seven patients with recurrent symptoms and increased resting left ventricular outflow tract pressure gradient (LVOTG) after PTSMA and another 14 patients with HOCM without history of PTSMA were studied. Both resting and dobutamine stress echocardiography, PTSMA and LVP were routinely performed.</p><p><b>RESULTS</b>In patients without previous PTSMA procedure, mild reduction of resting LVOTG was detected at 5 minutes after left ventricular pacing, and this reduction became significant at 10 minutes. All patients were divided into successful and unsuccessful groups according to their response to LVP. In contrary to patients in unsuccessful group, resting and R-S2 stimuli-induced LVOTG during PTSMA procedure were decreased dramatically ((9 +/- 5) mmHg vs (58 +/- 12) mmHg, (12 +/- 2) mmHg vs (113 +/- 27) mmHg, P < 0.001). Analysis of Logistic regression demonstrated that only LVOTG level during left ventricular pacing was an independent factor predicting the reduction of LVOTG immediately after PTSMA (odds ratio (OR), 0.59; 95% CI 2.67 to 5.82; P = 0.0002).</p><p><b>CONCLUSION</b>Left ventricular endocardial temporary pacing plays a critical role in predicting acute effect on the reduction of LVOTG immediately after PTSMA procedure.</p>