Circulation: Clinical Summaries
Original Research Put Into Perspective for the Practicing Clinician
- Relationship Between Vein Graft Failure and Subsequent Clinical Outcomes After Coronary Artery Bypass Surgery
- Phospholipase A2 Enzymes, High-Dose Atorvastatin, and Prediction of Ischemic Events After Acute Coronary Syndromes
- Air Pollution and Incidence of Hypertension and Diabetes Mellitus in Black Women Living in Los Angeles
- Cardiac Complications in Patients With Community-Acquired Pneumonia: Incidence, Timing, Risk Factors, and Association With Short-Term Mortality
- Impact of Progression of Diastolic Dysfunction on Mortality in Patients With Normal Ejection Fraction
- Proteomics Analysis of Cardiac Extracellular Matrix Remodeling in a Porcine Model of Ischemia/Reperfusion Injury
- Long-Term Propensity Score–Matched Comparison of Percutaneous Closure of Patent Foramen Ovale With Medical Treatment After Paradoxical Embolism
- Retrospective Analysis of Surgery Versus Endovascular Intervention in Takayasu Arteritis: A Multicenter Experience
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Relationship Between Vein Graft Failure and Subsequent Clinical Outcomes After Coronary Artery Bypass Surgery
In our study, we showed that the composite of death, myocardial infarction, or revascularization occurred more frequently among patients who had any vein graft failure compared with those who had none (adjusted hazard ratio, 1.58; 95% confidence interval, 1.21–2.06; P=0.008). This was due mainly to more frequent revascularization in patients with vein graft failure with no differences in death (adjusted hazard ratio, 1.04; 95% confidence interval, 0.71–1.52; P=0.85) or death or myocardial infarction (adjusted hazard ratio, 1.08; 95% confidence interval, 0.77–1.53; P=0.65) between patients with and without vein graft failure. Our findings suggest that the increased risk of repeat revascularization was not only from incidental findings on protocol-mandated angiography but also from clinical symptoms and/or objective evidence of ischemia. Vein graft failure rates were higher in patients with poor graft and target artery quality. The absolute number of failed grafts did not correlate with long-term clinical outcomes; however, the proportion of grafts with vein graft failure did. Emphasis should be directed toward selection of a good-quality vein conduit and preventing vein graft injury during harvesting. Beyond surgery, optimal secondary prevention, including medications and lifestyle modification, may have significant influence on prolonging vein graft patency and/or reducing clinical event rates in patients undergoing coronary artery bypass graft surgery. The high vein graft failure rate and its relationship with worse clinical outcomes call for more research on how to improve both short- and long-term vein graft patency in patients undergoing coronary artery bypass graft surgery. See p 749.
Phospholipase A2 Enzymes, High-Dose Atorvastatin, and Prediction of Ischemic Events After Acute Coronary Syndromes
Secretory phospholipase A2 (sPLA2) and lipoprotein-associated phospholipase A2 (Lp-PLA2) are enzyme biomarkers of increased cardiovascular risk and targets of emerging therapeutic agents. This study demonstrates that sPLA2 mass independently predicts death during a 16-week period after acute coronary syndrome (ACS). High-dose atorvastatin significantly reduces sPLA2 and Lp-PLA2 mass and activity after ACS and mitigates the risk of death associated with sPLA2 mass. Atorvastatin may exert antiinflammatory effects on phospholipases that contribute to its therapeutic benefit after ACS. These findings, derived from a large, randomized, placebo-controlled study and measuring sPLA2 and Lp-PLA2 mass and activity for the first time in the same data set, provide an important roadmap for interpreting future studies on sPLA2 and Lp-PLA2 inhibitors. The observations in this analysis are timely because novel inhibitors of Lp-PLA2 and sPLA2 are being evaluated for clinical efficacy in large, prospective, randomized trials involving patients with recent ACS (SOLID, VISTA-16). These inhibitors may reduce the mass and/or activity of these phospholipases. Since the completion of the Myocardial Ischemia Reduction With Aggressive Cholesterol Lowering (MIRACL) and Pravastatin or Atorvastatin Evaluation and Infection Therapy (PROVE-IT) trials, intensive statin treatment has become the standard of care after ACS. Therefore, future data sets will not provide the opportunity of the placebo-controlled MIRACL trial to assess both the natural history and prognostic value of phospholipase A2 biomarkers after ACS in the placebo arm and the modulation of these patterns by intensive statin treatment. See p 757.
Air Pollution and Incidence of Hypertension and Diabetes Mellitus in Black Women Living in Los Angeles
Hypertension affects >70 million adults in the United States and is the leading risk factor for premature mortality. The prevalence and adverse health consequences of type II diabetes mellitus are also large and continue to grow. Both disorders are causally related to cardiovascular diseases, the leading cause of mortality worldwide. Although lifestyle factors such as obesity, sedentary lifestyle, and poor diet play substantial roles in the development of diabetes mellitus and hypertension, emerging findings suggest that environmental exposures may predispose to both conditions. Our findings add to the evidence that present-day levels of ambient air pollution, specifically fine particulate matter with an aerodynamic diameter of ≤2.5 μm and nitrogen oxides, may contribute to the genesis of these chronic disorders. Although short-term exposures to particulate and traffic-related pollutants have been associated in many studies with acute cardiovascular events, the present results support the notion that longer-term exposures may promote the development of chronic diseases, specifically hypertension and diabetes mellitus. This may help explain the larger increase in mortality related to long-term versus short-term air pollution exposures. These observations could have major public health implications. Because of the ubiquitous and continuous exposures to air pollutants, even relatively small effects could potentially lead to serious elevations in the frequency of these disorders in the United States and globally. Our findings contribute to the evidence that characteristics of the environment, including neighborhood socioeconomic status and urban form, influence the development of chronic disease. Interventions aimed solely at the individual may not be sufficient to stem the increasing population prevalence of diabetes mellitus and hypertension. See p 767.
Cardiac Complications in Patients With Community-Acquired Pneumonia: Incidence, Timing, Risk Factors, and Association With Short-Term Mortality
Community-acquired pneumonia (CAP) is a common infection and a leading cause of morbidity and mortality that tends to occur in patients at high cardiovascular risk (ie, the elderly, smokers, diabetics, patients with chronic cardiac conditions). Community-acquired pneumonia can trigger acute cardiac complications. This study analyzed a prospective cohort of 2287 patients with community-acquired pneumonia in whom the 30-day incidence of cardiac complications was investigated. New or worsening heart failure, new or worsening arrhythmias, and myocardial infarction occurred in 20.8%, 11%, and 3% of inpatients and in 1.4%, 1%, and 0.1% of outpatients, respectively. Several patients had more than one of these conditions. Overall, cardiac complications (1 or more of the cardiac events above) were diagnosed in 27% and 2% of inpatients and outpatients, respectively. A majority of cardiac complications in both groups (89% inpatients and 75% outpatients) were diagnosed within the first week, more than half of them in the first 24 hours. Risk factors for cardiac complications included older age, nursing home residence, preexisting cardiovascular disease, and pneumonia severity. The occurrence of cardiac complications was associated with an adjusted 60% increase in risk of death at 30 days. Clinicians must recognize the burden of cardiac complications in patients with community-acquired pneumonia and exercise appropriate clinical alertness for their timely recognition. Rates of influenza and pneumococcal vaccination in groups of high cardiac risk need to be optimized. Further research to test risk stratification, prevention, and treatment strategies for incident cardiac complications in patients with community-acquired pneumonia may reduce the burden of death associated with this infection. See p 773.
Impact of Progression of Diastolic Dysfunction on Mortality in Patients With Normal Ejection Fraction
Diastolic dysfunction is an independent predictor of mortality in patients with normal ejection fraction. Diastolic function, whether normal or abnormal (stage 1, 2, or 3), varies dynamically and can pass from 1 stage to the other and in either direction. Although worsening of diastolic function has been associated with the development of congestive heart failure, there have been limited data on mortality with this progression. The present study showed that worsening of diastolic function in outpatients with normal ejection fraction (n=1065; age, 69±13 years) was associated with increased risk of death (hazard ratio, 1.78; 95% confidence interval, 1.21–2.59; P=0.003) independently of baseline or current diastolic function. This hazard ratio was equivalent to that from worsening of systolic function in the same population. Furthermore, progression from normal to abnormal diastolic function and from stage 1 to 2 or 3 diastolic dysfunction was associated with increased mortality (hazard ratio, 3.58; 95% confidence interval, 1.71–7.53; P=0.0001; and hazard ratio, 2.13; 95% confidence interval, 1.19–3.83; P=0.01, respectively). Given the present findings, it is important for clinicians not only to recognize the importance of progression of diastolic function for their patients but also to promote aggressive risk factor modifications, particularly blood pressure control, weight loss, exercise, and salt restriction; these risk factors have traditionally have been associated with worsening of diastolic function. See p 782.
Proteomics Analysis of Cardiac Extracellular Matrix Remodeling in a Porcine Model of Ischemia/Reperfusion Injury
By diverging from the traditional focus on intracellular proteins, we used a conceptually novel proteomics approach in which newly synthesized matrix proteins or loosely bound factors in the extracellular space were analyzed before the tissues were decellularized and integral extracellular matrix components were solubilized, which are not dissolved in conventional extraction buffers. By using this extraction procedure combined with state-of-the-art proteomics, we revealed novel extracellular matrix components in cardiac tissue and gained important insights into extracellular matrix remodeling by region and stage of fibrosis. Unlike any other proteomics study published to date, this extensive comparison allowed, for the first time, a coexpression analysis of extracellular matrix remodeling in a porcine model of myocardial ischemia/reperfusion injury. This biosignature of early- and late-stage remodeling may have clinical utility as prognostic markers. The novel extracellular matrix components identified in this study, and particularly those involved in the TGFβ regulatory pathway, may represent interesting modifiable targets for drug discovery. See p 789.
Long-Term Propensity Score–Matched Comparison of Percutaneous Closure of Patent Foramen Ovale With Medical Treatment After Paradoxical Embolism
The patent foramen ovale (PFO) is a recognized cause of stroke and systemic embolism, the mechanism being a venous clot that passes through the PFO and causes systemic ischemia. For about 20 years, PFOs have been closed percutaneously to prevent such events. The technique has matured and is now quite simple and safe. However, there is no evidence from randomized trials that this technique is safer than a conservative approach consisting of oral anticoagulation, platelet inhibitors, or a combination thereof. The data here represent the longest follow-up of 308 consecutive patients arbitrarily treated with PFO closure or medical therapy. In a propensity score–matched analysis, 103 patients with PFO closure were compared with 103 patients without PFO closure. At the mean follow-up of ≈10 years, a significant clinical event relatable to PFO occurred in 11% of patients with PFO closure and 21% of those without PFO closure (P=0.033). Transient ischemic attacks accounted for most of these events (5% and 14%, respectively). There were no complications with clinical sequelae in the PFO closure group. These data confirm other studies that PFO closure is safe; no late complications were found. The prevention of systemic ischemic events (particularly transient ischemic attacks) appears to be slightly superior to medical treatment. See p 803.
Retrospective Analysis of Surgery Versus Endovascular Intervention in Takayasu Arteritis: A Multicenter Experience
Aggressive medical and surgical treatment is required for patients with Takayasu arteritis suffering from major complications and a progressive disease course. With recent advances in endovascular treatment, percutaneous endoluminal angioplasty has become particularly attractive for arterial lesions of Takayasu arteritis. However, the data have come from small series, and the long-term outcome has not been reported. We conducted a retrospective study to report the long-term outcome of 79 consecutive patients with Takayasu arteritis who underwent 166 vascular procedures (surgery, 104 [62.7%]; endovascular repair, 62 [37.3%]) for the management of arterial complications. The overall 1- and 3-year rates of arterial complication were 22% and 33%, respectively. In multivariate analysis, we found an independent association of biological inflammation (odds ratio, 7.48; 95% confidence interval, 1.42–39.39) with the occurrence of postprocedural arterial complications. Our study suggests that biological inflammation at the time of revascularization increased the likelihood of complications in patients with Takayasu arteritis. See p 813.
- © 2012 American Heart Association, Inc.
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