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INSIDE THIS ISSUE

Inside This Issue

	State-of-the-Art Paper

Top State-of-the-Art Paper Viewpoint Clinical Research Pre-Clinical Research

Peter Libby, Paul M. Ridker, Göran K. Hansson, for the Leducq Transatlantic Network on Atherothrombosis

Libby and colleagues describe the recent transition in the understanding of atherosclerosis from a bland proliferative process to an active one involving multiple components of the body's immune system. Those various components are reviewed in this paper, which begins with an overview of the important roles that both innate and cellular immunity play. The interaction between inflammation and thrombosis is also discussed. This review also discusses how translation of these advances in understanding the pathophysiology may change clinical practice, either through the use of biomarkers, such as high-sensitivity C-reactive protein, or novel agents that target specific actors in the inflammatory cascade.

	Viewpoint

Top State-of-the-Art Paper Viewpoint Clinical Research Pre-Clinical Research

 
Viewpoint.   A Half Century of Selective Coronary Arteriography

2139

Albert V. G. Bruschke, William C. Sheldon, Earl K. Shirey, William L. Proudfit

The first "selective" coronary arteriogram was made 50 years ago by Dr. F. Mason Sones at the Cleveland Clinic. Soon afterward, coronary arteriography was suitable for widespread clinical application. This has revolutionized our understanding of coronary artery disease and has become the basis for selecting and evaluating therapeutic interventions. This paper by Bruschke and colleagues commemorates the achievements of the pioneers of coronary arteriography, reviews the difficulties they encountered, and highlights their impact on the development of modern cardiology.

	Clinical Research

Top State-of-the-Art Paper Viewpoint Clinical Research Pre-Clinical Research

 
Interventional Cardiology.   CMR Study Demonstrates Benefits of Prompt Primary PCI

2145

Marco Francone, Chiara Bucciarelli-Ducci, Iacopo Carbone, Emanuele Canali, Raffaele Scardala, Francesca A. Calabrese, Gennaro Sardella, Massimo Mancone, Carlo Catalano, Francesco Fedele, Roberto Passariello, Jan Bogaert, Luciano Agati

Francone and colleagues investigated the relationship between myocardial damage and time to reperfusion using cardiovascular magnetic resonance (CMR) in patients with ST-segment elevation myocardial infarction who underwent primary percutaneous coronary intervention (PCI). Myocardial edema and necrosis were quantified as the area at risk and infarct size, respectively; salvaged myocardium was defined as the difference between the two. Shorter time to reperfusion (<90 min) was associated with smaller infarct size and larger salvaged myocardium. Salvaged myocardium markedly decreased when reperfusion occurred >90 min after symptom onset. Time to reperfusion determines the extent of reversible and irreversible myocardial injury, with 90 min from symptom onset being an important threshold.

Editorial Comment: Richard W. Smalling, p. 2154

Interventional Cardiology.   One Dose of Atorvastatin Reduces Rates of Periprocedural MI
2157

Carlo Briguori, Gabriella Visconti, Amelia Focaccio, Bruno Golia, Alaide Chieffo, Alfredo Castelli, Marco Mussardo, Matteo Montorfano, Bruno Ricciardelli, Antonio Colombo

Some data suggests that statins can reduce the rates of periprocedural myocardial infarction (MI) in patients undergoing percutaneous coronary intervention (PCI). Briguori and colleagues hypothesized that this benefit is due to their "pleiotropic" effects, independent of cholesterol reduction, and that this benefit could develop within 24 h. Statin-naive subjects undergoing elective PCI were randomized to either a single 80-mg dose of atorvastatin, given within 24 h of the procedure, or usual care. Periprocedural MI, defined as a creatine kinase-myocardial isoenzyme elevation >3 times the upper limit of normal, occurred in 9.5% of the atorvastatin group and 15.8% of the control group. Similar reductions were found with troponin elevation. A single dose of atorvastatin reduces the incidence of periprocedural MI in elective PCI.

Editorial Comment: Sotirios Tsimikas, p. 2164

Coronary Artery Disease.   Autopsy Study: Microemboli and Microvascular Obstruction After Acute Coronary Thrombosis

2167

Robert S. Schwartz, Allen Burke, Andrew Farb, David Kaye, John R. Lesser, Timothy D. Henry, Renu Virmani

Schwartz and colleagues studied the histopathology of epicardial coronary artery plaque in patients dying from coronary artery occlusion and its relationship to microemboli and microvascular obstruction. Hearts from patients experiencing sudden coronary death underwent a histopathologic examination. There were 26 plaque ruptures and 21 plaque erosions in these 44 hearts, with a mean of 4.5 microemboli per heart. Vascular microemboli and microvascular obstruction occurred more often from plaque showing erosion rather than rupture, but intramyocardial microemboli were more common after plaque rupture. Microemboli and microvascular obstruction are common in patients dying of acute coronary thrombosis caused by plaque erosion.

Biomarkers.   Soluble ST2 Predicts Risk of SCD in Patients With Chronic Heart Failure

2174

Domingo A. Pascual-Figal, Jordi Ordoñez-Llanos, Pedro L. Tornel, Rafael Vázquez, Teresa Puig, Mariano Valdés, Juan Cinca, Antoni Bayes de Luna, MAntoni Bayes-Genis, on behalf of the MUSIC Investigators

Pascual-Figal and colleagues used a large registry of patients with heart failure to determine if the soluble form of ST2 (sST2), an interleukin-1 receptor family member, predicts the risk of sudden cardiac death (SCD). A nested case-control study was performed on 36 cases of SCD and 63 controls (matched for age, sex, and left ventricular ejection fraction) enrolled in a registry of ambulatory heart failure patients. Concentrations of sST2 were higher among those who died. Combining sST2 and N-terminal pro–B-type natriuretic peptide (NT-proBNP) improved the accuracy: only 4% of patients with low sST2 and low NT-proBNP experienced SCD. The rate was 34% when either marker was elevated and 71% when both markers were elevated. sST2 may be useful for predicting the risk of SCD, especially when combined with NT-proBNP.

Congenital Heart Disease.   Percutaneous Stenting Compared to the Blalock-Taussig Shunt

2180

Giuseppe Santoro, Giovanbattista Capozzi, Giuseppe Caianiello, Maria Teresa Palladino, Chiara Marrone, Gabriella Farina, Maria Giovanna Russo, Raffaele Calabrò

This study sought to determine if arterial duct (AD) stenting or a modified Blalock-Taussig shunt (MBTS) was more successful at stimulating growth in the pulmonary arteries (PAs) in neonates with congenital heart disease with duct-dependent pulmonary circulation. Subjects who had undergone one of the procedures were compared. The PA growth was angiographically assessed using a variety of indexes, and the right-to-left PA diameter ratio was measured as a surrogate of uniform growth. After 10 months, both options had promoted a significant increase in PA size; however, the surgical shunt caused a worsening of the left-to-right PA diameter ratio due to growth of the PA contra-lateral to the shunt. Percutaneous AD stenting appears to be as effective as MBTS in promoting PA growth and may result in more balanced pulmonary vascular development.

	Pre-Clinical Research

Top State-of-the-Art Paper Viewpoint Clinical Research Pre-Clinical Research

 
Pre-Clinical Research.   ALDH2 Ameliorates Acute Cardiac Toxicity of Ethanol
2187

Heng Ma, Ji Li, Feng Gao, Jun Ren

Ma and colleagues hypothesized that acetaldehyde, which is the first metabolic product of ethanol, may be the toxic factor that causes alcoholic cardiomyopathy. They tested this hypothesis by generating a strain of transgenic mice with cardiac overexpression of mitochondrial aldehyde dehydrogenase-2 (ALDH2), which breaks down acetaldehyde. Wild-type and ALDH2 mice were injected with ethanol (3 g/kg, intraperitoneally), and cardiac function was assessed 24 h later using both Langendroff and cardiomyocyte edge-detection systems. The deteriorations in myocardial and cardiomyocyte contractile function were alleviated by ALDH2. Furthermore, ethanol-induced myocardial apoptosis, protein damage, and mitochondrial membrane potential depolarization were lessened in ALDH2 mice. This study demonstrates that ALDH2 may be protective against acute ethanol-induced cardiac toxicity.

Editorial Comment: Joel S. Karliner, p. 2197

Related Articles

Inflammation in Atherosclerosis: From Pathophysiology to Practice

Peter Libby, Paul M. Ridker, Göran K. Hansson for the Leducq Transatlantic Network on Atherothrombosis
J. Am. Coll. Cardiol. 2009 54: 2129-2138. [Abstract] [Full Text] [PDF]

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