Medical and surgical treatment of acute right ventricular failure.

Acute right ventricular (RV) failure is a frequent and serious clinical challenge in the intensive care unit. It is usually seen as a consequence of left ventricular failure, pulmonary embolism, pulmonary hypertension, sepsis, acute lung injury or after cardiothoracic surgery. The presence of acute RV failure not only carries substantial morbidity and mortality, but also complicates the use of commonly used treatment strategies in critically ill patients. In contrast to the left ventricle, the RV remains relatively understudied, and investigations of the treatment of isolated RV failure are rare and usually limited to nonrandomized observations. We searched PubMed for papers in the English language by using the search words right ventricle, right ventricular failure, pulmonary hypertension, sepsis, shock, acute lung injury, cardiothoracic surgery, mechanical ventilation, vasopressors, inotropes, and pulmonary vasodilators. These were used in various combinations. We read the abstracts of the relevant titles to confirm their relevance, and the full papers were then extracted. References from extracted papers were checked for any additional relevant papers. This review summarizes the general measures, ventilation strategies, vasoactive substances, and surgical as well as mechanical approaches that are currently used or actively investigated in the treatment of the acutely failing RV.

Predictors of weight change in overweight patients with myocardial infarction.

BACKGROUND: Weight loss is recommended among overweight survivors of myocardial infarction (MI). This study describes patterns of weight change among overweight patients with MI and identifies factors associated with weight change. METHODS: A prospective cohort of 1253 overweight or heavier (body mass index [BMI] > or = 25 kg/m2) post-MI patients were enrolled in the 19-center PREMIER study and followed up for 1 year to determine changes in weight. Patients were categorized at 1 month as overweight (BMI = 25-29.9 kg/m2), obese (BMI = 30-39.9 kg/m2), or morbidly obese (BMI > or = 40 kg/m2). Unadjusted percent weight change was assessed at 1 year, and multivariable linear regression was used to identify independent correlates of change. RESULTS: Mean weight change was -0.2% and varied by the severity of baseline obesity (+0.4% for overweight patients, -0.5% for obese patients, and -3.7% for morbidly obese patients [P < .001]). Multivariable analyses revealed the following to be significantly associated with weight change: depression 1 month post-MI (+2.7%, P = .001), lack of health insurance (+2%, P = .01), smoking cessation 1 month post-MI (+2.7% vs current smokers, P < .001), morbid obesity (+4.7% vs overweight patients, P < .0001), and increasing age (-0.8% per decade, P = .001). An interaction between smoking cessation and weight class was detected in that overweight patients who quit had a mean increase of 5.3% (95% CI 3.1%-7.4%), whereas no significant change was observed among obese and morbidly obese patients who quit. CONCLUSIONS: Although post-MI patients had negligible weight loss over 1 year, several sociodemographic, clinical, and lifestyle characteristics were associated with weight change. New, targeted interventions will likely be needed to improve weight management after an MI.

A review of spinal injuries in the invasive cardiologist: part 1. Biomechanics and pain generation.

This review provides a perspective of spinal injuries related to invasive cardiology, an understanding of the anatomy and physiology of the spine, the etiology and pathophysiology of spinal injuries, and options for prevention and treatment. Because of the breadth of this review, it has been divided into two parts with the first describing the biomechanics and generation of back pain and the second discussing treatment options and prevention of back injury. A comprehensive overview of the biomechanics of the spine from the individual vertebral unit to the complex motions involved in everyday life is reviewed. The significant intrinsic and extrinsic factors playing a role in the mechanism of disc damage, including occupational hazards encountered by the invasive cardiologist, are discussed. We also address the mechanisms of pain generation in the spine and the role that inflammation plays, which explains the presence of symptoms with little or no detectable pathology on imaging studies.

A review of spinal injuries in the invasive cardiologist II: prevention and treatment.

This review provides a perspective of spinal injuries related to invasive cardiology, an understanding of the anatomy and physiology of the spine, the etiology and pathophysiology of spinal injuries, and options for prevention and treatment. In this part of our review, conventional surgical and minimally invasive options are discussed as well as emerging techniques for the treatment of back pain. We also discuss methods of preventing back injuries by modifications to the work environment as well as preventive measures that may be practiced by the invasive cardiologist. Our final objective is to describe and illustrate proven techniques for strengthening the supportive musculature to avoid spinal injury as well as to reduce painful exacerbations.

History of hypertension and enhanced thrombogenic activity in postinfarction patients.

Hypertension is a risk factor for coronary thrombosis and death in cardiac patients mediated in part by endothelial damage or dysfunction and increased thrombogenicity. However, there are no data regarding the association between hypertension and thrombogenic activity in stable patients after myocardial infarction and limited data about the prognostic significance of thrombogenic factors in hypertensive patients after infarction. Therefore, levels of thrombogenic, lipid, and inflammatory factors were measured 2 months after an acute myocardial infarction in 461 hypertensive and 582 nonhypertensive patients. Thrombogenic factors included d-dimer, fibrinogen, plasminogen activator inhibitor-1, von Willebrand factor, factor VII, and factor VIIa. Lipid variables included cholesterol (total, HDL, LDL), triglyceride, lipoprotein (a), apolipoprotein-A1, and apolipoprotein-B. The prognostic significance of these factors for predicting cardiac events during a 2-year follow-up was evaluated in hypertensive and nonhypertensive patients. In comparison with nonhypertensive patients, those with hypertension had higher levels of d-dimer (607 versus 453 mg/L, P<0.001), fibrinogen (3.64 versus 3.43 g/L, P<0.001), plasminogen activator inhibitor-1 (29.7 versus 27.3 ng/mL, P=0.01), von Willebrand factor (159 versus 141 IU/dL; P<0.001), and higher levels of inflammatory markers (hsCRP and SAA). In multivariate analysis after adjustment for clinical covariates, elevated d-dimer was the only factor independently associated with a history of hypertension (OR, 1.38, P=0.05). d-Dimer was associated with an increased risk of recurrent cardiac events in both hypertensive (hazard ratio=3.02, P=0.005) and nonhypertensive (hazard ratio=2.42, P=0.02) patients. Thus, patients after infarction with a history of hypertension have enhanced thrombogenic activity, which predisposes them to recurrent cardiac events.