Sustained ventricular arrhythmias and mortality among patients with acute myocardial infarction: Results from the GUSTO-III trial

2003 ◽  
Vol 145 (3) ◽  
pp. 515-521 ◽  
Author(s):  
Sana M. Al-Khatib ◽  
Amanda L. Stebbins ◽  
Robert M. Califf ◽  
Kerry L. Lee ◽  
Christopher B. Granger ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Ventricular Arrhythmias

Adjacent QT dispersion: A good predictor of ventricular arrhythmias after myocardial infarction

Open Medicine ◽  
2008 ◽  
Vol 3 (2) ◽  
pp. 179-182 ◽  
Author(s):  
Mohammad Ostovan ◽  
Shahdad Khosropanah ◽  
Shohreh Hooshmand
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Qt Interval ◽  
Regional Variation ◽  
Ventricular Arrhythmias ◽  
Qt Dispersion ◽  
Maximum Difference ◽  
Simple Method ◽  
Qtc Dispersion ◽  
Surface Electrocardiogram

AbstractThe 12-lead surface electrocardiogram adjacent QTc dispersion, which is the maximum difference of corrected QT interval between two adjacent leads, is a simple method to determine regional variation in repolarization and refractoriness. The aim of this study is to evaluate adjacent QTc dispersion as a marker of susceptibility to ventricular arrhythmias after myocardial infarction. A total of 135 consecutive patients with acute myocardial infarction were enrolled in the study. Adjacent QTc, measured by lens magnifier, was calculated on the first, second and third days after acute myocardial infarction. On the second day after acute myocardial infarction, adjacent QTc dispersion was significantly greater in patients with ventricular arrhythmias (P < 0.001). Adjacent QTc dispersion on the first and fifth day after acute myocardial infarction was not associated with development of ventricular arrhythmias. On the second day after acute myocardial infarction, adjacent QTc dispersion is a simple and feasible method for prediction of ventricular arrhythmias.

P1603Nicorandil suppresses ischemia-induced cardiac interstitial norepinephrine enhancement and ventricular arrhythmia in hypertrophic hearts

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M Kobara ◽  
N Naseratun ◽  
Y Watanabe ◽  
H Toba ◽  
T Nakata
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Ventricular Tachycardia ◽  
Ventricular Arrhythmia ◽  
Ventricular Arrhythmias ◽  
Sham Group ◽  
Cardiac Tissue ◽  
Norepinephrine Release ◽  
Norepinephrine Concentration ◽  
Ischemic Period

Abstract Background Myocardial infarction (MI) is a major cause of death in western countries and Japan, and hypertension is a major risk factor of MI. In hypertensive heart, acute myocardial infarction often leads to lethal ventricular arrhythmia. Nicorandil, an ATP sensitive potassium channel (KATP) opener, is usually used in the treatment of acute myocardial infarction. The effects of nicorandil on ischemic myocyte are fully defined. On the other hand, KATP in neuroterminals is known to regulate norepinephrine release, but the effect of nicorandil on ischemic norepinephrine release in cardiac tissue has remained unexplored. Purpose We examined whether nicorandil suppressed norepinephrine release via neuronal KATP and ventricular arrhythmia during acute ischemia in pressure overload-induced hypertrophic hearts. Methods SD Rats were divided into two groups; abdominal aortic constriction (AAC) group and sham-operated (Sham) group. Four weeks after constriction, cardiac geometry and function were examined using echocardiography. Then, myocardial ischemia was induced by the left anterior descending artery occlusion for 100 minutes in the presence or absence of intravenous infusion of nicorandil. Cardiac interstitial norepinephrine concentration in ischemic region was measured using the microdialysis method and concentration of cyclic AMP, a second messenger of norepinephrine, in cardiac tissue was measured by ELISA. Ventricular arrhythmias were monitered by ECG during whole ischemic period. Results Four weeks after constriction, remarkable left ventricular wall thickening was observed in AAC group. Before ischemia, ventricular arrhythmia was not found in both groups. Number of ventricular arrhythmia, including ventricular tachycardia and ventricular fibrillation, was increased in early ischemic period (- 40 min) in both groups, and was grater in AAC group. Before ischemia, interstitial norepinephrine concentration in cardiac tissue was higher level in AAC group than in Sham group. Ischemia obviously increased norepinephrine concentration in both groups time dependently and AAC further increased norepinephrine than Sham group. Concentration of cyclic AMP in cardiac tissue was raised in early ischemic period (- 40 min) and then gradually decreased. Nicorandil significantly suppressed the number of ventricular arrhythmias, and abolished the ventricular tachycardia and fibrillation without hemodynamic alterations. Nicorandil also attenuated norepinephrine and cAMP enhancement in acute ischemic period in both groups. Conclusion Ischemia-induced ventricular arrhythmia was more frequent and severe in hypertrophic hearts and interstitial norepinephrine enhancement may play a role in this ischemic arrhythmia. Nicorandil suppressed ischemia-induced interstitial norepinephrine release by neuronal KATP opening, which attenuated ventricular arrhythmias in normal and hypertrophic hearts.

Small Doses of Subcutaneous Heparin, Plasma Free-Fatty-Acids, and the Incidence of Ventricular Arrhythmias in Patients with Acute Myocardial Infarction

1979 ◽  
Author(s):  
H. Arnesen ◽  
Ø. Skjæggestad ◽  
N. Wik
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Fatty Acids ◽  
Free Fatty Acids ◽  
Ventricular Arrhythmias ◽  
Prospective Trial ◽  
Plasma Free Fatty Acids ◽  
Vein Thrombosis ◽  
Subcutaneous Heparin ◽  
Small Doses

The frequency of deep vein thrombosis (DVT) diagnosed with the 125I-fibrinogen technique in patients with acute myocardial infarction (AMI) has been found to be reduced frcm about 20% without anticoagulation to about 5% with warfarin or small doses of subcutaneous heparin.A somewhat higher incidence of ventricular tachycardia in patients with AMI treated with small doses of subcutaneous heparin has been reported. A possible mechanism might be heparin-induced activation of lipoprotein lipase with consequent increase of plasma free-fatty-acids (FFA), which have been found to be arrhythmogenic in patients with AMI.In the present prospective trial, 99 patients with AMI and a history of less than 12 hours were allocated at random to treatment with subcutaneous heparin 5000 IU twice daily, or warfarin. In a randomized subsample of 21 patients fasting FFA analyses were performed before and 2 hours after the administration of anticoagulants on day 1 and 2.No measurable increase in FFA concentrations was demonstrated in the heparin-treated patients, in spite of a significant influence on the thrombin clotting time.The frequency of ventricular arrhythmias as detected by continous tape recordings was equal in the two treatment groups.It is concluded that subcutaneous heparin 5 000 IU every 12 hours seems to be a safe measures of prophylaxis against venous thromboembolic ccmplications in patients with AMI.

scholarly journals Thrombin Receptor and Ventricular Arrhythmias after Acute Myocardial Infarction

2008 ◽  
Vol 14 (3-4) ◽  
pp. 131-140 ◽  
Author(s):  
Lilong Tang ◽  
Chunyu Deng ◽  
Ming Long ◽  
Anli Tang ◽  
Shulin Wu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Ventricular Arrhythmias ◽  
Thrombin Receptor

Genetic Variants on SCN5A, KCNQ1, and KCNH2 in Patients with Ventricular Arrhythmias during Acute Myocardial Infarction in a Chinese Population

Cardiology ◽  
2019 ◽  
Vol 145 (1) ◽  
pp. 38-45 ◽  
Author(s):  
Feng Wang ◽  
Yang Liu ◽  
Hongtao Liao ◽  
Yumei Xue ◽  
Xianzhang Zhan ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Association Study ◽  
Chinese Population ◽  
Ventricular Arrhythmias ◽  
Rare Variants ◽  
Allelic Frequency ◽  
Genotype Frequency ◽  
Missense Variants ◽  
Significant Difference

Objective: Acute myocardial infarction (AMI) remains a leading cause of morbidity and mortality worldwide. About half of sudden deaths from AMI are mainly because of malignant ventricular arrhythmias (VA) after AMI. The sodium channel gene SCN5A and potassium channel genes KCNQ1 and KCNH2 have been widely reported to be genetic risk factors for arrhythmia including Brugada syndrome and long QT syndrome (LQTS). A few studies reported the association of SCN5A variant with ventricular tachycardia (VT)/ventricular fibrillation (VF) complicating AMI. However, little is known about the role of KCNQ1 and KCNH2 in AMI with VA (AMI_VA). This study focuses on investigating the potential variants on SCN5A, KCNQ1, and KCNH2 contributing to AMI with VA in a Chinese population. Materials and Methods: In total, 139 patients with AMI_VA, and 337 patients with AMI only, were included. Thirty exonic sites were selected to be screened. Sanger sequencing was used to detect variants. A subsequent association study was also performed between AMI_VA and AMI. Results: Twelve variants [5 on KCNH2(NM_000238.3), 3 on KCNQ1(NM_000218.2), and 4 on SCN5A(NM_198056.2)] were identified in AMI_VA patients. Only 5 (KCNH2: c.2690A>C; KCNQ1: c.1927G>A, c.1343delC; SCN5A: c.1673A>G, c.3578G>A) of them are missense variants. Two (KCNQ1: c.1343delC and SCN5A: c.3578G>A) of the missense variants were predicted to be clinically pathogenic. All these variants were further genotyped in an AMI without VA group. The association study identified a statistically significant difference in genotype frequency of KCNH2: c.1539C>T and KCNH2: c.1467C>T between the AMI and AMI_VA groups. Moreover, 2 rare variants (KCNQ1: c.1944C>T and SCN5A: c.3621C>T) showed an elevated allelic frequency (more than 1.5-fold) in the AMI_VA group when compared to the AMI group. Conclusion: Twelve variants (predicting from benign/VUS to pathogenic) were identified on KCNH2, KCNQ1, and SCN5A in patients with AMI_VA. Genotype frequency comparison between AMI_VA and AMI identified 2 significant common variants on KCNH2. Meanwhile, the allelic frequency of 2 rare variants on KCNQ1 and SCN5A, respectively, were identified to be enriched in AMI_VA, although there was no statistical significance. The present study suggests that the ion-channel genes KCNH2, KCNQ1, and SCN5A may contribute to the pathogenesis of VA during AMI.

Sign in / Sign up

Export Citation Format

Share Document