INSIDE THIS ISSUE OF JACC
Inside This Issue of JACC
 |
Acute Myocardial Infarction
|
|---|
Coronary Plaque Temperature Measurement Can Identify Culprit Lesions.
Plaque rupture leading to vessel occlusion may produce proximal thrombosis, which might obscure the location of the initial area of rupture during angiography. Takumi and colleagues measured arterial wall temperatures and compared these to intravascular ultrasound (IVUS) and angiographic images in 45 patients with anterior acute myocardial infarction (AMI). In patients with total vessel occlusion, the maximal temperature (Tmax) site was 8 to 10 mm more distal to the angiographically occlusive site; for those with reperfusion, the mean distance was 1.1 mm. When a culprit plaque could be identified by IVUS, it correlated with the area of highest temperature. Temperature measurement of the coronary arterial wall can identify the culprit plaque in AMI and confirms that proximal thrombus may mask the initial culprit lesion. See page 2197. See figure.
|
Acute Myocardial Infarction
|
|---|
Coxsackie Infection May Increase Risk of Fatal MI.
Coxsackievirus-B (CV-B) serotypes are known to persistently infect human myocytes and vascular endothelial cells, but the pathological significance of this is unclear. Andréoletti and colleagues assessed myocardial sections obtained at autopsy from patients dying of acute myocardial infarction (AMI) versus those dying of noncoronary cardiac disease or of other causes. Positive immunostaining for the capsid viral protein 1 was present in 40% of patients dying of AMI, which was 15 times higher than in patients dying from accidental causes and 7 times higher than in those dying of noncoronary cardiac disease. This study shows for the first time the presence of an active CV-B infection in a high proportion of patients with AMI. See page 2207. See figure.
|
Cardiac Pharmacology
|
|---|
Tolerance to NTG Linked to Inhibition of ALDH-2 and Reactive Oxygen Species.
Hink and colleagues hypothesized that inhibition of the nitroglycerin bioactivating enzyme mitochondrial aldehyde dehydrogenase (ALDH-2) contributes to nitroglycerin (NTG) tolerance. They analyzed mammary artery sections and saphenous vein sections harvested during bypass surgery in patients treated with intravenous NTG for >48 h prior to surgery versus those with no NTG exposure. Arteries from patients treated with NTG showed a lack of vasodilation in response to NTG, which was mimicked by incubation of nontolerant vessels with an ALDH-2 inhibitor. Furthermore, patients treated with NTG showed decreased expression and activity of ALDH-2; ALDH-2 activity could be restored by incubation with a sulfhydryl group donor, suggesting that reactive oxygen species are the etiology. This study suggests that NTG use promotes production of reactive oxygen species that decreases ALDH-2 activity, which leads to decreased efficacy of NTG. See page 2226. See figure.
|
Heart Rhythm Disorders
|
|---|
Driving Appears to be Safe for Those With ICDs.
The safety of driving for patients with a history of ventricular tachycardia (VT) or ventricular fibrillation (VF) is unclear. The TOVA (Triggers of Ventricular Arrhythmia) study compared the risk of implantable cardioverter-defibrillator (ICD) shock for VT/VF both during and up to 60 min after driving. The absolute risk of ICD shock for VT/VF within 1 h of driving was estimated to be 1 episode per 25,116 person-hours spent driving, and there was only 1 accident associated with an arrhythmia. The risk of shocks for VT/VF occurred primarily during the 30-min period following driving (relative risk = 4.46) rather than during the driving episode itself (relative risk = 1.05). Although the risk of ICD shock for VT/VF was transiently increased in the 30-min period after driving, the risk was not elevated during driving and the absolute risk was low, suggesting that patients with ICDs are safe to drive. See page 2233.
Related Articles
-
Limitation of Angiography to Identify the Culprit Plaque in Acute Myocardial Infarction With Coronary Total Occlusion: Utility of Coronary Plaque Temperature Measurement to Identify the Culprit Plaque
- Takuro Takumi, Souki Lee, Shuichi Hamasaki, Kouichi Toyonaga, Daisuke Kanda, Keisuke Kusumoto, Hitoshi Toda, Toshihiro Takenaka, Masaaki Miyata, Ryuichiro Anan, Yutaka Otsuji, and Chuwa Tei
J. Am. Coll. Cardiol. 2007 50: 2197-2203.
[Abstract]
[Full Text]
[PDF]
-
Active Coxsackieviral B Infection Is Associated With Disruption of Dystrophin in Endomyocardial Tissue of Patients Who Died Suddenly of Acute Myocardial Infarction
- Laurent Andréoletti, Lydie Ventéo, Fatima Douche-Aourik, Frédéric Canas, Geoffroy Lorin de la Grandmaison, Jérôme Jacques, Hélène Moret, Nicolas Jovenin, Jean-François Mosnier, Mathieu Matta, Sébastien Duband, Michel Pluot, Bruno Pozzetto, and Thomas Bourlet
J. Am. Coll. Cardiol. 2007 50: 2207-2214.
[Abstract]
[Full Text]
[PDF]
-
Oxidative Inhibition of the Mitochondrial Aldehyde Dehydrogenase Promotes Nitroglycerin Tolerance in Human Blood Vessels
- Ulrich Hink, Andreas Daiber, Nalan Kayhan, Jordis Trischler, Catharina Kraatz, Matthias Oelze, Hanke Mollnau, Philip Wenzel, Christian F. Vahl, Kwok Ki Ho, Henry Weiner, and Thomas Munzel
J. Am. Coll. Cardiol. 2007 50: 2226-2232.
[Abstract]
[Full Text]
[PDF]
-
Driving and Implantable Cardioverter-Defibrillator Shocks for Ventricular Arrhythmias: Results From the TOVA Study
- Christine M. Albert, Lawrence Rosenthal, Hugh Calkins, Jonathan S. Steinberg, Jeremy N. Ruskin, Paul Wang, James E. Muller, Murray A. Mittleman for the TOVA Investigators
J. Am. Coll. Cardiol. 2007 50: 2233-2240.
[Abstract]
[Full Text]
[PDF]
Top
Acute Myocardial Infarction
Acute Myocardial Infarction
