| ||||||||||||||||||||||||||||||||||||||||||||||||||||
(Circulation. 2004;110:3157.)
© 2004 American Heart Association, Inc.
Issue Highlights
EXCESSIVE TUMOR NECROSIS FACTOR ACTIVATION AFTER INFARCTION CONTRIBUTES TO SUSCEPTIBILITY OF MYOCARDIAL RUPTURE AND LEFT VENTRICULAR DYSFUNCTION, by Sun et al.
Forming a stable scar in the heart after a myocardial infarction is analogous to replacing a flat tire without pulling over into the breakdown lane. Given the requirement for constant cardiac work during the wound repair, it is surprising that cardiac rupture does not occur more often as a fatal complication of infarction. In this issue of Circulation, Sun et al dissect the process of postinfarction wound repair using mice lacking the cytokine tumor necrosis factor-
. Their exciting results provide new insight into the process of cardiac scar formation after transmural infarction. In addition, their findings suggest some potential strategies to limit the risk of cardiac rupture that may resuscitate the concept of targeting cytokines for the treatment of heart disease. See p 3221.
PULMONARY HYPERTENSION AND RIGHT HEART FAILURE IN PITUITARY ADENYLATE CYCLASE–ACTIVATING POLYPEPTIDE TYPE I RECEPTOR–DEFICIENT MICE, by Otto et al.
Pulmonary hypertension, characterized by vasoconstriction, remodeling of the pulmonary vasculature, and thrombosis, often results in right heart failure because of continually elevated pulmonary artery pressures. The etiology of pulmonary hypertension is multifactorial, and several genetic, molecular, and cellular factors all have been shown to contribute to the pathophysiological features of pulmonary hypertension. Otto et al now extend this list by demonstrating that mice deficient in PAC1, the pituitary adenylate cyclase activating polypeptide (PACAP)-preferring type-1-receptor, develop pulmonary hypertension and severe right heart failure after birth. These studies implicate PAC1 as a critical determinant in cardiopulmonary regulation and identify PAC1 as a candidate molecule for future therapeutic interventions. See p 3245.
RIGHT VENTRICULAR ENLARGEMENT ON CHEST COMPUTED TOMOGRAPHY: A PREDICTOR OF EARLY DEATH IN ACUTE PULMONARY EMBOLISM, by Schoepf et al.
Contrast-enhanced chest computed tomography (CT) increasingly is used for diagnosis of acute pulmonary embolism. Newer-generation scanners also allow standard views and assessment of cardiac function, including right ventricular function, which can be visualized and quantified more routinely than with echocardiography. In their study in this issue, Schoepf and colleagues show that right ventricular enlargement, as imaged by contrast-enhanced chest CT, in patients with acute pulmonary embolism is a powerful predictor of short-term (30-day) mortality. These data suggest that the now widely available CT provides not only important diagnostic information, but also prognostic information about short-term risk of death for such patients. These data will help inform the always challenging decision making about the need for thrombolytic or high-risk surgical management of patients with acute pulmonary embolism. See p 3276.
Visit www.circ.ahajournals.org:
Images in Cardiovascular Medicine
Isolated Right Ventricular Infarction Resulting From Occlusion of a Nondominant Right Coronary Artery. See p e500.
Double-Chambered Left Ventricle: Complete Characterization by Cardiac Magnetic Resonance and Multidetector-Row Computed Tomography. See p e502.
Book Review
Surgical Foundations: Essentials of Thoracic Surgery. See p e504.
Correspondence
|
Related Articles:
Circulation 2004 110: 3221-3228.
Circulation 2004 110: 3245-3251.
Circulation 2004 110: 3276-3280.
Circulation 2004 110: e500-e501.
Circulation 2004 110: e502-e503.
Circulation 2004 110: e504.
| ||||||||||||||||||||||||||||||||||||||||||||||||||||