Prevalence and variability in reporting of clinically actionable incidental findings on attenuation-correction CT scans in a veteran population.

BACKGROUND: Myocardial perfusion imaging (MPI) often employs attenuation-correction computed tomography (CTAC) to reduce attenuation artifacts and improve specificity. While there is no specific guideline on how they should be reported, incidental noncardiac findings identified on these scans may be clinically significant. The prevalence of these findings in veterans is not currently known. In addition, variability in reporting these findings may depend on the interpreting physician's specialty. METHODS: To guide future decision-making, CTACs in veterans referred for MPI were prospectively evaluated in a quality-control project for a set of prespecified actionable incidental findings by cardiologists and a radiologist. RESULTS: On the 771 scans performed over eight months, 285 incidental noncardiac findings were identified by the interpreting cardiologists and 378 were identified by the interpreting radiologist. Pulmonary nodules were the most common occurring in 20% of studies read by the radiologist. Interreader agreements between cardiologists and the radiologist were poor for pulmonary nodules ≥ 10 mm and hiatal hernias; fair for pulmonary nodules < 10 mm, extracardiac masses, and aortic aneurysms; and moderate for pleural plaques. CONCLUSION: Incidental noncardiac findings on CTACs are common in our veteran population. Overall interobserver agreement in identifying these findings between cardiologists and radiologists is fair. Specific guidelines are needed on how CTACs should be read and reported.

Contemporary approach to stroke prevention in atrial fibrillation: Risks, benefits, and new options.

Atrial fibrillation is a common diagnosis affecting nearly 3 million adults in the United States. Morbidity and mortality in these patients is driven largely by the associated increased risk of thromboembolic complications, especially stroke. Atrial fibrillation is a stronger risk factor than hypertension, coronary disease, or heart failure and is associated with an approximately five-fold increased risk. Mitigating stroke risk can be challenging and requires accurate assessment of stroke risk factors and careful selection of appropriate therapy. Anticoagulation, including the more recently introduced direct oral anticoagulants, is the standard of care for most patients. In addition, emerging non-pharmacologic mechanical interventions are playing an expanding role in reducing stroke risk in select patients. In this review we highlight the current approach to stroke risk stratification in atrial fibrillation and discuss in detail the mechanism, risks, and benefits of current and evolving therapies.

Derivation of a Clinical Model to Predict Unchanged Inpatient Echocardiograms.

BACKGROUND: Transthoracic echocardiography (TTE) is one of the most commonly ordered tests in healthcare. Repeat TTE, defined as a TTE done within 1 year of a prior TTE, represents 24% to 42% of all studies. The purpose of this study was to derive a clinical prediction model to predict unchanged repeat TTE, with the goal of defining a subset of studies that are unnecessary. METHODS: Single-center retrospective cohort study of all hospitalized patients who had a repeat TTE between October 1, 2013, and September 30, 2014. RESULTS: Two hundred eleven of 601 TTEs were repeat studies, of which 78 (37%) had major changes. Five variables were independent predictors of major new TTE changes, including history of intervening acute myocardial infarction, cardiothoracic surgery, major new electrocardiogram (ECG) changes, prior valve disease, and chronic kidney disease. Using the ß-coefficient for each of these variables, we defined a clinical prediction model that we named the CAVES score. The acronym CAVES stands for chronic kidney disease, acute myocardial infarction, valvular disease, ECG changes, and surgery (cardiac). The prevalence of major TTE change for the full cohort was 35%. For the group with a CAVES score of -1, that probability was only 5.6%; for the group with a score of 0, the probability was 17.7%; and for the group with a score ≥1, the probability was 55.3%. The bootstrap corrected C statistic for the model was 0.78 (95% confidence interval, 0.72-0.85), indicating good discrimination. CONCLUSIONS: Overall, the CAVES score had good discrimination and calibration. If further validated, it may be useful to predict repeat TTEs that are unlikely to have major changes.

Multi-modality molecular imaging of aortic aneurysms.

Aneurysms of the thoracic and abdominal aorta are common and can be associated with significant morbidity and mortality when complications, including dissection, rupture, or thrombosis, occur. Current approaches to diagnosis and risk stratification rely on measurements of aneurysm size and rate of growth, often using various imaging modalities, which may be suboptimal in identifying patients at the highest and lowest risk of complications. Targeting the biological processes underlying aneurysm formation and expansion with molecular imaging offers an exciting opportunity to characterize aortic aneurysms beyond size and address current gaps in our approach to diagnosis and treatment. In this review, we summarize the epidemiology and biology of aortic aneurysms and highlight the role of molecular imaging in furthering our understanding of aneurysm pathogenesis and its potential future role in guiding management.

Acute Myocardial Infarction from Coronary Vasospasm Precipitated by Pseudoephedrine and Metoprolol Use.

Pseudoephedrine is a sympathomimetic α- and ß-adrenergic receptor agonist that causes vasoconstriction and reduction in edema throughout the nasal passages. Coronary vasospasm associated with pseudoephedrine has been reported in the literature. We discuss the case of a patient with new-onset atrial fibrillation receiving metoprolol for rate control on a background of pseudoephedrine use for allergic rhinitis leading to acute myocardial infarction from multivessel coronary vasospasm. This case illustrates the importance of understanding the pharmacology of potential drug-drug interactions when managing patients with acute cardiovascular syndromes.

Hibernating myocardium retains metabolic and contractile reserve despite regional reductions in flow, function, and oxygen consumption at rest.

Hibernating myocardium, characterized by reductions in flow and function at rest, has limited contractile reserve in response to increases in external workload. We hypothesized that this attenuation of function reflects an adaptive downregulation that prevents the development of metabolic evidence of ischemia during stress. To test this hypothesis, pigs were chronically instrumented with a proximal left anterior descending artery stenosis for 3 months, resulting in severe anteroapical hypokinesis with reduced resting perfusion (0.78+/-0.05 versus 0.94+/-0.07 mL x min(-1)x g(-1) in remote, P<0.01; and 0.99+/-0.08 in controls, P<0.05). Open-chest studies confirmed resting dysfunction compared with normal controls (segment shortening 9.2+/-2.2% versus 23.5+/-1.1%, P<0.05). Resting myocardial oxygen consumption was reduced (63+/-3 versus 77+/-6 microL x g(-1) x min(-1) in controls, P<0.05), yet lactate consumption was normal. Although subendocardial perfusion failed to increase during graded, intravenous epinephrine infusion (n=8), peak segment shortening (to 17.3+/-3.1%, P<0.05) and oxygen consumption (to 90+/-6 microL x g(-1) x min(-1), P<0.01) increased from the depressed resting levels. There was no lactate production in hibernating myocardium, and lactate uptake increased during stress (0.7+/-0.1 to 1.2+/-0.1 micromol x g(-1) x min(-1), P<0.05). The absence of metabolic evidence of ischemia was also confirmed during atrial pacing to a rate of 120 bpm (n=8). Thus, despite reductions in function and oxygen consumption at rest, hibernating myocardium retains the ability to increase metabolism without the development of acute ischemia. This supports the hypothesis that the downregulation of oxygen consumption and function in hibernating myocardium is an adaptive response that prevents a supply-demand imbalance during submaximal increases in cardiac workload when coronary flow reserve is limited.

Variability of contractile reserve in hibernating myocardium: dependence on the method of inotropic stimulation.

OBJECTIVE: Contractile reserve during graded beta-adrenergic stimulation identifies viability in patients with left ventricular dysfunction. Nevertheless, contractile reserve is frequently absent in viable, chronically dysfunctional myocardium with reduced resting flow (hibernating myocardium). The goal of this study was to evaluate the mechanisms responsible for limited contractile reserve in hibernating myocardium. METHODS: Pigs were chronically instrumented with a left anterior descending coronary artery (LAD) stenosis to produce hibernating myocardium; and regional flow, function and hemodynamics were assessed during graded beta-adrenergic stimulation (epinephrine). RESULTS: The chronic LAD stenosis produced a critical reduction in coronary flow reserve with regional reductions in resting subendocardial flow (0.69+/-0.05 vs. 1.03+/-0.11 ml/min/g in shams, P<0.05) and wall thickening (2.0+/-0.4 vs. 4.3+/-0.4 mm in shams, P<0.05), consistent with hibernating myocardium. In sham controls, LAD flow and function increased during graded, steady-state increases in epinephrine. Nevertheless, despite similar external determinants of demand in animals with hibernating myocardium, neither subendocardial flow (peak response: 0.66+/-0.14 and peak dose: 0.58+/-0.13 ml/min/g, respectively) nor wall thickening (3.0+/-0.5 and 2.5+/-0.6 mm, respectively) increased during graded epinephrine infusion. However, during a transient epinephrine infusion to the maximum dose used in the graded protocol, flow remained unchanged (0.80+/-0.06 to 0.85+/-0.08 ml/min/g) but wall thickening improved (2.3+/-0.4 to 4.1+/-0.6 mm, P<0.05). CONCLUSIONS: These data indicate that variability in contractile reserve in hibernating myocardium is at least partly related to the protocol used for beta-adrenergic stimulation. The blunted steady-state responses to beta-adrenergic stimulation raise the possibility that, like moderate supply-induced ischemia, an exquisite matching between flow and function develops during moderate demand-induced ischemia. This prevents metabolic deterioration in hibernating myocardium but limits contractile function during increases in the external determinants of myocardial metabolism.