BACKGROUND Coronary artery disease (CAD) patients experience chest pain (CP) from cardiac and non-cardiac etiologies. OBJECTIVE Proton pump inhibitor (PPI) treatment of CAD patients with atypical CP would result in less CP, as well as fewer emergency room (ER) visits for CP, medical evaluations, and hospitalizations. METHODS A randomized, prospective, placebo-controlled trial in patients with a history of severe CAD, without current ischemia, and not receiving acid reducing therapy. Patients received esomeprazole 40 mg or placebo daily added to standard cardiac medications for 6 months. The primary endpoint was percentage of patients experiencing CP. RESULTS In 162 patients randomized, 78 received esomeprazole and 84 received placebo. Esomeprazole significantly reduced the primary endpoint of patients experiencing CP (24.4% versus 54.8%; p < 0.001). The absolute number of CP episodes and CP days was also significantly reduced. Fewer patients experienced the combined endpoint of doctor office/ER visits for CP (19.2% versus 48.8%; p < 0.001), mainly due to significantly fewer office visits for CP (14.1% versus 39.3%; p < 0.001). ER visits for CP trended less with esomeprazole (12.8% versus 22.6%; p = 0.10), as did hospitalizations for CP (14.1% versus 20.2%; p = 0.30). However, the study lacked statistical power to reach these secondary endpoints. CONCLUSIONS Concomitant esomeprazole therapy in CAD patients without active ischemia but with a history of atypical CP reduces number of patients with further CP symptoms and medical office visits for CP. Larger studies are needed to further evaluate PPI treatment on ER CP visits and hospitalizations in this patient population.

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.

Background: Patients with coronary artery disease presenting to an emergency department with chest pain are likely to undergo hospitalization in an attempt to elucidate its aetiology.Aim: To examine whether coronary artery disease patients receiving proton-pump inhibitor therapy are associated with fewer chest pain events and evaluations.Methods: A veteran patient population with documented coronary artery disease was identified, and chest pain episodes, emergency department visits and hospitalizations for chest pain were followed over 2 years. Patient outcomes between proton-pump inhibitor use and non-use of proton-pump inhibitor therapy were compared.Results: In 415 male patients, 23% utilized a proton-pump inhibitor and 77% did not. Proton-pump inhibitor therapy was associated with fewer chest pain episodes (12% vs. 26%, P = 0.002), emergency department visits, ( 12% vs. 24%, P = 0.044) and hospitalizations (13% vs. 24%, P = 0.086). The incidence of adverse events was decreased in the proton-pump inhibitor group: 70% fewer chest pain episodes ( P 0.002, RR = 3.3), 55% fewer emergency department visits (P = 0.049, RR = 2.2) and 53% fewer hospitalizations (P = 0.064, RR = 2.1). By multivariate analysis, proton-pump inhibitor therapy independently predicted a reduced prevalence of patients experiencing chest pain, emergency department visits, and hospitalizations [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 veteran coronary artery disease patients is associated with fewer chest pain episodes, emergency department visits and hospitalizations for chest pain.

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.

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.

Improvements in coronary stents have made planned direct coronary stenting technically feasible, though safety, acute success, cost‐effectiveness, and long‐term results remain to be determined. Sequential patients eligible for direct stenting were prospectively characterized and treated with either direct or secondary stenting. Major adverse cardiovascular events (MACE) such as cardiac death, myocardial infarction (MI), target vessel ischemia, or revascularization (TVR) were followed for 6 months post‐PCI. Enrollment included 128 direct (1.38 lesions/patient) and 69 secondary (1.39 lesions/patient) stented patients. Direct stenting was successful in 99% (with 5% crossover to secondary stenting) without major procedural complications and with a similar rate of vessel wall dissection or no‐reflow phenomenon (2.3% vs. 2.1%; P > 0.05) as the secondary stenting group. There was a trend toward less postprocedural CPK‐MB elevation in the nonacute MI patients with direct vs. secondary stenting (3% vs. 11%, respectively). At 6 months, there were no statistically significant differences in overall MACE. Direct stenting has a high success rate, low complication rate, and durable long‐term results. Procedural cost and time savings, less contrast use and radiation exposure make direct stenting attractive in properly selected patients. Cathet Cardiovasc Intervent 2001;54:158–163. © 2001 Wiley‐Liss, Inc.