Simultaneous papillary muscle avulsion and free wall rupture during acute myocardial infarction. Intra-aortic balloon pump: a bridge to survival.

Mechanical complications of acute myocardial infarction (AMI) are rare, but often fatal. Medical therapy does not provide adequate risk reduction, and surgical correction is recommended when feasible. Supplemental hemodynamic support utilizing intra-aortic counterpulsation with a balloon pump provides an improvement in morbidity and mortality when combined with a corrective surgical approach. We report a case of an elderly male with a progressive 2-week history of ischemic symptoms presenting with acute pulmonary edema, hypotension and an inferior wall ST-elevation MI. His hospital course was complicated by ischemic mitral regurgitation (MR) and cardiogenic shock, which resulted in a papillary muscle rupture/avulsion from the inferolateral myocardial wall, and a communication for blood from ventricle to pericardial space. Initial management included mechanical ventilation, pharmacologic inotropic support, percutaneous revascularization of the culprit lesion and intra-aortic balloon counterpulsation. The patient underwent further successful cardiovascular surgical correction of his incompetent mitral valve, free wall rupture and other obstructive coronary arteries, leading to discharge and survival. Mechanical complications from AMI and the role of intra-aortic balloon support are discussed.

Proton pump inhibitors for patients with coronary artery disease associated with reduced chest pain, emergency department visits, and hospitalizations.

BACKGROUND: Patients with coronary artery disease (CAD) presenting to an emergency department (ED) with chest pain are likely to undergo hospitalization as clinicians attempt to elucidate the etiology. HYPOTHESIS: We hypothesized that proton pump inhibitor (PPI) therapy is associated with reduced chest pain events and evaluations in patients with CAD. METHODS: A patient population from a veterans medical center with documented CAD was identified retrospectively, and chest pain episodes, ED visits, and hospitalizations for chest pain were prospectively followed over 2 years. Comparison of patient outcomes between PPI (+PPI) and nonuse of PPI therapy (-PPI) was determined. RESULTS: Of 415 male patients, average age 73.4 years, 23% utilized a PPI and 77% did not. Proton pump inhibitor therapy was associated with reduced chest pain episodes (11.8 vs. 26.2%, p = 0.002), ED visits (12.3 vs. 24.3%, p = 0.044), and hospitalizations (12.8 vs. 23.9%, p = 0.086). Relative reductions were 55, 49, and 46%, respectively, after 2 years. Numbers of adverse events were also decreased in the +PPI group of patients: 70% fewer occurrences of chest pain (p = 0.002, relative risk [RR] = 3.3), 55% fewer ED visits (p = 0.049, RR = 2.2), and 53% fewer hospitalizations (p = 0.064, RR = 2.1). By multivariate analysis, PPI therapy independently predicted reduced prevalence of patients experiencing chest pain, ED visits, or hospitalizations (odds ratio [OR] = 0.09 [0.04-0.21]; 0.15 [0.06-0.40]; 0.14 [0.05-0.40]; all p < 0.001). CONCLUSIONS: Proton pump inhibitor therapy for male patients with CAD from a veterans medical center was associated with reduced prevalence of chest pain, ED visits, and hospitalizations for chest pain and reduced incidence of these events.

Sirolimus- and taxol-eluting stents differ towards intimal hyperplasia and re-endothelialization.

Restenosis is a direct result of vessel injury, local inflammation, and remodeling following balloon angioplasty and coronary stenting resulting in luminal narrowing. The process involves a complex interplay of released growth factors that stimulate smooth muscle cells (SMCs) to migrate and proliferate, as well as activating endothelial cells (ECs) at injury sites. The latter re-establishes the luminal endothelial monolayer that keeps a barrier to circulating cells from underlying extracellular matrix and SMCs. Understanding the cellular mechanisms of intimal hyperplasia and re-endothelialization is important in that uncontrolled cellular processes account for coronary luminal narrowing, leading to the recurrence of clinical symptoms, hospitalizations, and repeat interventions. The evolution of drug-eluting stents that inhibit intimal hyperplasia has revolutionized percutaneous coronary interventions in that potential late luminal narrowing is attenuated. Sirolimus and paclitaxel are two medications utilized for their efficacy at inhibiting intimal hyperplasia and subsequent clinical events. The effects of these drugs on EC biology have not been well investigated. This article discusses basic cellular processes of vessel repair after balloon angioplasty and stenting, and focuses on the differential molecular mechanisms of sirolimus and paclitaxel towards proliferation and migration. These drugs inhibit both SMC and EC proliferation, but by different mechanisms, and paclitaxel inhibits EC migration, whereas sirolimus does not. Their discriminating effects towards re-endothelialization may clinically differentiate these two drugs. Inhibiting re-endothelialization may translate into more adverse clinical events.

Chest pain from gastroesophageal reflux disease in patients with coronary artery disease.

Management of patients with coronary artery disease is a major challenge for physicians, patients, and the healthcare system. Chest pain experienced by patients with coronary disease can be of noncardiac origin, and symptoms frequently related to gastroesophageal etiologies. The distal esophagus and the heart share a common afferent nerve supply, suggesting that location and radiation of perceived pain may be identical. In addition, there is substantial overlap between the prevalence of coronary disease and gastroesophageal reflux disease. Many physicians, including cardiologists, prescribe acid-reducing therapy to coronary patients. However, no prospective, randomized studies to date have evaluated the potential benefit of such treatments to prevent chest pain symptoms for these patients. We review the studies on noncardiac chest pain demonstrating reflux in patients with and without coronary disease. Also, the association of reflux with exertional chest pain and cardiac syndrome X is discussed. A rationale is presented for prevention of noncardiac chest pain in coronary patients, and the potential role of acid-suppressive therapy in managing these patients is discussed.

Triple valve repair for rheumatic heart disease.

The onset of the clinical expression of rheumatic heart disease (RHD) is variable. Exercise or other states that necessitate increased cardiac output often precipitate symptoms. Mitral stenosis (MS) is present in 25% of patients with RHD, and 40% of patients have concomitant MS and mitral regurgitation. About two third of patients with MS have concurrent aortic insufficiency. Pulmonary and tricuspid insufficiency may occur from rheumatic involvement of these valves, or secondary to dilatation of valve annuli from pulmonary hypertension secondary to mitral and/or aortic valve disease. Pregnancy is associated with many hemodynamic changes including expanded intravascular volume, tachycardia, increased intracardiac dimensions, and valvular regurgitation. We report a case of a young female who developed flash pulmonary edema during parturition and was found to have abnormal rheumatic involvement of her aortic, mitral, and tricuspid valves. Successful triple valve repair was performed in a single operation. A review of rheumatic valvular abnormalities, and literature supporting multivalvular repair for rheumatic heart disease is provided.