Current methods to assess mitral annular calcification and its risk factors.

INTRODUCTION: Mitral annulus calcification (MAC) is a chronic, non-inflammatory, degenerative mechanism of the fibrous base of the mitral valve. While MAC was originally thought to be an age-related degenerative process, there is evidence that other mechanisms, such as atherosclerosis and abnormal calcium phosphorus metabolism, also contribute to the development of MAC. AREAS COVERED: This paper summarizes, existing perception of clinically valid definition of MAC and the pathophysiological processes that lead to the development of MAC and the diagnostic implications of this disease entity. EXPERT OPINION: Minimal evidence exists on the natural history and progression of MAC. Characterization of MAC progression and identification of predisposing risk factors can help to validate hypotheses. MAC is most commonly asymptomatic and incidental finding. Echocardiography is the primary imaging modality for identification and characterization of MAC and associated mitral valve (MV) disease. For patients with an indication for MV surgery, computed tomography (CT) is a complementary imaging modality for MAC. MAC is generally recognized by its characteristic density, location, and shape on echocardiography and CT, unusual variants are sometimes confused with other lesions.

The Quantification of Total Coronary Atheroma Burden - A Major Step Forward.

The extent of coronary artery disease has been shown to be an important indicator of prognosis. Cardiac computed tomography (CT) has the ability to measure plaque, with both coronary artery calcium scanning and CT angiography (CTA), to give a measure of total atheroma burden. Beyond assessing stenosis and atherosclerosis, CTA can assess high-risk plaque. These plaques are thought to be consistent with plaques that are vulnerable and more likely to rupture and cause acute coronary syndromes. However, the high-risk plaque concept suffers from poor reproducibility and poor positive predictive power. Total coronary atheroma burden has been shown to be a better predictor of coronary events than high-risk plaques or stenosis. This paper reviews the literature in this regard and demonstrates total coronary atheroma burden to be the best predictor of future cardiovascular disease. We searched MEDLINE, EMBASE and the Cochrane library database for studies assessing plaque burden and outcomes by CT. We used text words and related Medical Subject Headings (MeSH) for cardiac, calcification, plaque burden, CT, prognosis, mortality, event, death, survival and myocardial infarction.

Tumor necrosis factor α inhibitor use and decreased risk for incident coronary events in rheumatoid arthritis.

OBJECTIVE: To determine the association of tumor necrosis factor α (TNFα) inhibitors with risk for cardiovascular disease (CVD) in rheumatoid arthritis (RA) patients. METHODS: A retrospective cohort of 2,101 incident RA patients was established. Medication exposure was categorized into the following groups: TNFα inhibitors alone or in combination with methotrexate (MTX; aTNF group); MTX alone or in combination with other nonbiologic disease-modifying antirheumatic drugs (DMARDs; MTX group); and no MTX, nonbiologic DMARDs (reference group). Primary outcome was adjudicated incident coronary artery disease (CAD), defined as myocardial infarction, unstable angina, or coronary revascularization procedure. Secondary outcome was adjudicated incident CVD, defined as a composite of CAD, stroke, transient ischemic attack, abdominal aortic aneurysm, peripheral arterial disease, or arterial revascularization procedure. Cox regression models were used to calculate the hazard ratio for CAD and CVD for the aTNF and MTX groups compared to the reference group. RESULTS: There were 46 incident CAD and 82 incident CVD events. Adjusting for covariates associated with CAD and CVD, the hazard ratio for incident CAD was 0.45 (95% confidence interval [95% CI] 0.21-0.96) for the aTNF group and 0.54 (95% CI 0.27-1.09) for the MTX group compared to the reference group. Use of TNFα inhibitors for >16.1 months was associated with a relative risk for CAD of 0.18 (95% CI 0.06-0.50) and for CVD of 0.31 (95% CI 0.15-0.65) compared to the reference group. A similar, although not significant, trend was seen with the MTX group. CONCLUSION: Use of TNFα inhibitors is associated with a decreased risk for CAD in RA; the risk decreases further with long-term use. This should be considered when weighing the risks versus benefits of these medications.

Dobutamine-induced myocardial ischemia and ST-segment elevation in collateral-dependent myocardium.

In patients with obstructive coronary artery disease, electrocardiographic (ECG) ST-segment elevation (STE) is frequently seen during dobutamine stress echocardiography (DSE) in leads overlying previous transmural left ventricular (LV) myocardial infarction. The mechanism of occasional STE during DSE in LV region with inducible myocardial ischemia and no previous myocardial infarction has not been well delineated. We retrospectively identified 28 adults (age 51 to 83 years [69 ± 8]; 82% men) with STE (>1 mm at ≥80 ms after J point in ≥2 contiguous leads without pathologic Q waves) and inducible myocardial ischemia in the same territory during DSE. STE occurred in inferior (n = 16), inferolateral (n = 8), anterior (n = 1), lateral (n = 2), or anterolateral (n = 1) leads and was associated with ischemic symptoms in 17 patients (61%). Inducible LV wall motion abnormality developed in LV segments corresponding to ECG STE in all patients. Coronary arteriography (within 1 week of the index DSE) showed severe luminal narrowing in the major epicardial coronary artery supplying the region with DSE STE and ischemia (90% to 99% in 9 patients [32%] and 100% in 19 patients [68%]). The ischemic region was supplied by ipsilateral (n = 4 [14%]), contralateral (n = 21 [75%]), or both ipsilateral and contralateral (n = 3 [11%]) collateral branches. In conclusion, dobutamine-induced ECG STE in LV segments with normal baseline wall motion is a highly reliable marker of viable collateral-dependent myocardium.

Perioperative beta blockers in patients having non-cardiac surgery: a meta-analysis.

BACKGROUND: American College of Cardiology and American Heart Association (ACC/AHA) guidelines on perioperative assessment recommend perioperative beta blockers for non-cardiac surgery, although results of some clinical trials seem not to support this recommendation. We aimed to critically review the evidence to assess the use of perioperative beta blockers in patients having non-cardiac surgery. METHODS: We searched Pubmed and Embase for randomised controlled trials investigating the use of beta blockers in non-cardiac surgery. We extracted data for 30-day all-cause mortality, cardiovascular mortality, non-fatal myocardial infarction, non-fatal stroke, heart failure, and myocardial ischaemia, safety outcomes of perioperative bradycardia, hypotension, and bronchospasm. FINDINGS: 33 trials included 12 306 patients. beta blockers were not associated with any significant reduction in the risk of all-cause mortality, cardiovascular mortality, or heart failure, but were associated with a decrease (odds ratio [OR] 0.65, 95% CI 0.54-0.79) in non-fatal myocardial infarction (number needed to treat [NNT] 63) and decrease (OR 0.36, 0.26-0.50) in myocardial ischaemia (NNT 16) at the expense of an increase (OR 2.01, 1.27-3.68) in non-fatal strokes (number needed to harm [NNH] 293). The beneficial effects were driven mainly by trials with high risk of bias. For the safety outcomes, beta blockers were associated with a high risk of perioperative bradycardia requiring treatment (NNH 22), and perioperative hypotension requiring treatment (NNH 17). We recorded no increased risk of bronchospasm. INTERPRETATION: Evidence does not support the use of beta-blocker therapy for the prevention of perioperative clinical outcomes in patients having non-cardiac surgery. The ACC/AHA guidelines committee should soften their advocacy for this intervention until conclusive evidence is available.