Niranjan Seshadri

Emergency Coronary Artery Bypass Surgery in the Contemporary Percutaneous Coronary Intervention Era

Background—Since the advent of percutaneous coronary interventions (PCIs), technological advances, adjunctive pharmacotherapy, and increasing operator experience have contributed to lowering the occurrence of major complications. However, emergency coronary artery bypass surgery (CABG) for failed PCI is still associated with important morbidity and mortality, even in the era of coronary stenting. We sought to determine the prevalence, indications, predictors, and complications of emergency CABG after PCI in the past decade. Methods and Results—We reviewed 18 593 PCIs performed from 1992 through 2000. There was a need for emergency CABG in 113 (0.61%) cases. The major indications were extensive dissection (n=61, 54%), perforation/tamponade (n=23, 20%), and recurrent acute closure (n=23, 20%). Prevalence of emergency CABG decreased from 1.5% of PCIs in 1992 to 0.14% in 2000 (P <0.001). Independent predictors of the need for emergency CABG included the worst ACC/AHA scoring of the intervened lesion (P <0.001) and female sex (P = 0.028), whereas history of prior bypass surgery and use of stents resulted in a decreased need for emergency CABG (P <0.001 for both). In patients undergoing emergency CABG, there were 17 (15%) in-hospital deaths, 14 (12%) perioperative Q-wave myocardial infarctions, and 6 (5%) cerebrovascular accidents. Conclusions—The need for emergency CABG has considerably decreased over time. Risk factors include female sex and a higher ACC/AHA score of the intervened lesion. However, morbidity and mortality of emergency CABG remain high even in the new millennium.

HOMOCYSTEINE, B VITAMINS, AND CORONARY ARTERY DISEASE

This article discusses the metabolism of homocysteine, factors affecting its plasma level, and the evidence for its role in the pathogenesis of vascular disease. The treatment of hyperhomocysteinemia and its possible impact on vascular disease prevention and progression are described also.

Pulmonary vein isolation for treatment of atrial fibrillation: Recent updates

Atrial fibrillation is the most common arrhythmia encountered by clinicians, with an estimated prevalence of 0.4% in the general population. Patients with nonrheumatic atrial fibrillation have a 2to 7-fold higher incidence of embolic stroke and have a mortality rate that is twice that of people in normal sinus rhythm.1 Traditional approaches to the management of atrial fibrillation include rate control and anticoagulation, chemical and electrical cardioversion, and in very symptomatic patients, AV nodal ablation and permanent pacemaker implantation. Recently, there has been much interest in more novel therapeutic approaches to atrial fibrillation, namely, catheter based mapping and ablation. The shift in focus to catheter based interventional techniques was in part inspired by the success of the surgical Maze procedure. Attempts were made to replicate the surgical Maze procedure by creating ablation lines in anatomically defined locations in both atria. The results of these catheter-based Maze procedures, however, have been disappointing. Haissaguerre et al.,2 in a seminal study, suggested that the ectopic beats originating in the pulmonary veins may be the triggers for atrial fibrillation. It seemed plausible that electrical isolation of ectopic foci originating in the pulmonary veins from rest of the atrial tissue would result in sustained cure. Over the last few years, rapid technological strides have been made in this area. This article will update the reader on recent technological advances and future directions in this field.

Pulmonary Vein Stenosis After Catheter Ablation of Atrial Arrhythmias

A 78-year-old woman presented with a 2-month history of worsening dyspnea, orthopnea, and cough with hemoptysis. Her past medical history was significant for hypertension and severe mitral regurgitation for which she had undergone mitral valve repair 3 years previously. In addition, she had recurrent atrial tachycardia requiring 2 radiofrequency ablations, which included ablation of several left-sided pathways. The last ablation was performed 3 months before her presentation. A transesophageal echocardiogram was performed and showed turbulent Doppler flow and increased systolic and diastolic velocities in the right lower (Figure 1) and left upper pulmonary veins. A …

Relation of albumin/creatinine ratio to C-reactive protein and to the metabolic syndrome.

We hypothesized that the association of high sensitivity C-reactive protein (CRP) with urinary albumin excretion (UAE) is predominately mediated through its correlation with the metabolic syndrome. Serum CRP and urine albumin:creatinine ratios (ACR) from 720 preventive cardiology patients were analyzed to estimate age- and gender-adjusted relative risk of high CRP and metabolic syndrome for high ACR. These data demonstrate that CRP independently predicts the presence of UAE, a marker of endothelial dysfunction.

Usefulness of plasma vitamin B6, B12, folate, homocysteine, and creatinine in predicting outcomes in heart transplant recipients

Atherothrombotic complications are frequently seen in patients undergoing heart transplantation. These patients have high plasma total homocysteine concentrations associated with lower folate and vitamin B(6) levels. The relation between these metabolic abnormalities and the development of vascular complications, however, remains unclear. Fasting plasma total homocysteine, folate, vitamin B(12), vitamin B(6), and creatinine were measured in 160 cardiac transplant recipients who were followed for a mean duration of 28 +/- 9 months after blood draw (mean 59 +/- 28 months after transplant). Cardiovascular events and causes of mortality were determined and Cox proportional-hazards regression analysis was used to identify the independent predictors for cardiovascular events and mortality. Twenty-five patients developed cardiovascular events and 17 died (11 cardiovascular deaths). Mean +/- SD total homocysteine value was 18.4 +/- 8.5 (range 4.3 to 63.5 micromol/L). Hyperhomocysteinemia (> or =15 micromol/L) was seen in 99 patients (62%). Levels were no different in patients with or without cardiovascular complications/death (16.8 +/- 6.2 vs 18.9 +/- 9 micromol/L, p = 0.4). However, vitamin B(6) deficiency was seen in 21% of recipients with and in 9% without cardiovascular complications/death (p = 0.05). The relative risk for cardiovascular events, including cardiovascular death, increased 2.7 times (confidence interval 1.2 to 5.9) for B(6) levels < or =20 nmol/L compared with those with normal B(6) levels (p = 0.02). Thus, hyperhomocysteinemia is common in transplant recipients but may have no causal role in the atherothrombotic vascular complications of transplantation. Deficiency of vitamin B(6), however, may predict adverse outcomes, suggesting a possible role for supplementation with this vitamin.

Dysregulation of endogenous carbon monoxide and nitric oxide production in patients with advanced ischemic or nonischemic cardiomyopathy

Carbon monoxide (CO) and nitric oxide (NO) are endogenous vasoregulatory molecules whose role in heart failure is not fully known. Exhaled CO and NO measurement provide novel noninvasive assessment of their endogenous production. We compared exhaled CO and NO in 24 patients with advanced ischemic and nonischemic cardiomyopathy and in 13 control subjects without known cardiac disease at rest and at 1 and 5 minutes after exercise testing. Exhaled CO was lower in patients with cardiomyopathy at rest (1.66 +/- 0.2 vs 1.80 +/- 0.5 ppm, p = 0.02) and 1 minute after exercise (1.35 +/- 0.2 vs 1.81 +/- 0.5 ppm, p = 0.009), with a similar trend at 5 minutes after exercise (1.45 +/- 0.3 vs 1.81 +/- 0.5 ppm, p = 0.14). Exhaled CO decreased in patients with cardiomyopathy after exercise (p <0.001 and p = 0.02 at rest vs 1 and 5 minutes after exercise, respectively) but was maintained in controls. Exhaled NO did not differ between patients with cardiomyopathy and controls at rest (9.48 +/- 1.4 vs 9.68 +/- 1.5 ppb, p = NS) and after exercise (1 minute: 10.91 +/- 1.8 vs 9.19 +/- 1.2 ppb; 5 minutes: 10.52 +/- 1.5 vs 8.90 +/- 1.2 ppb, p = NS). Exhaled NO increased after exercise in patients with cardiomyopathy (p = 0.01 and p = 0.04 rest vs exercise at 1 and 5 minutes, respectively), but was maintained in controls. Exhaled CO and NO were not correlated with peak oxygen consumption in patients with cardiomyopathy. The differential responses in exhaled CO and NO at rest or with exercise between patients with cardiomyopathy and normal controls may point to dysregulation in endogenous CO and NO production.