Impact of Cardiovascular Risk on the Relative Benefit and Harm of Intensive Treatment of Hypertension.

BACKGROUND: The lower rate of primary outcome events in the intensive treatment group in SPRINT (Systolic Pressure Intervention Trial) was associated with increased clinically significant serious adverse events (SAEs). In 2017, the American College of Cardiology/American Heart Association issued risk-based blood pressure treatment guidelines. The authors hypothesized that stratification of the SPRINT population by degree of future cardiovascular disease (CVD) risk might identify a group which could benefit the most from intensive treatment. OBJECTIVES: This study investigated the effect of baseline 10-year CVD risk on primary outcome events and all-cause SAEs in SPRINT. METHODS: Stratifying by quartiles of baseline 10-year CVD risk, Cox proportional hazards models were used to examine the associations of treatment group with the primary outcome events and SAEs. Using multiplicative Poisson regression, a predictive model was developed to determine the benefit-to-harm ratio as a function of CVD risk. RESULTS: Within each quartile, there was a lower rate of primary outcome events in the intensive treatment group, with no differences in all-cause SAEs. From the first to fourth quartiles, the number needed to treat to prevent primary outcomes decreased from 91 to 38. The number needed to harm for all-cause SAEs increased from 62 to 250. The predictive model demonstrated significantly increasing benefit-to-harm ratios (± SE) of 0.50 ± 0.15, 0.78 ± 0.26, 2.13 ± 0.73, and 4.80 ± 1.86, for the first, second, third, and fourth quartile, respectively (p for trend <0.001). All possible pairwise comparisons of between-quartile mean values of benefit-to-harm ratios were significantly different (p < 0.001). CONCLUSIONS: In SPRINT, those with lower baseline CVD risk had more harm than benefit from intensive treatment, whereas those with higher risk had more benefit. With the 2017 American College of Cardiology/American Heart Association blood pressure treatment guidelines, this analysis may help providers and patients make decisions regarding the intensity of blood pressure treatment.

Dabigatran-Induced Spontaneous Hemopericardium and Cardiac Tamponade.

Four novel oral anticoagulant agents are currently available for the prevention and treatment of thromboembolic events in patients with nonvalvular atrial fibrillation. We present an unusual case of spontaneous hemopericardium and tamponade in an 87-year-old man with atrial fibrillation who was taking one such agent, dabigatran, as thromboprophylaxis. Our case highlights both a rare bleeding complication of dabigatran use and the effectiveness of idarucizumab, its newly approved reversal agent. Especially in elderly patients, we recommend that clinicians evaluate risk factors, closely monitor patient status, and consider alternatives to the newer anticoagulants when the risk of bleeding is high.

Patient management after noninvasive cardiac imaging results from SPARC (Study of myocardial perfusion and coronary anatomy imaging roles in coronary artery disease).

OBJECTIVES: This study examined short-term cardiac catheterization rates and medication changes after cardiac imaging. BACKGROUND: Noninvasive cardiac imaging is widely used in coronary artery disease, but its effects on subsequent patient management are unclear. METHODS: We assessed the 90-day post-test rates of catheterization and medication changes in a prospective registry of 1,703 patients without a documented history of coronary artery disease and an intermediate to high likelihood of coronary artery disease undergoing cardiac single-photon emission computed tomography, positron emission tomography, or 64-slice coronary computed tomography angiography. RESULTS: Baseline medication use was relatively infrequent. At 90 days, 9.6% of patients underwent catheterization. The rates of catheterization and medication changes increased in proportion to test abnormality findings. Among patients with the most severe test result findings, 38% to 61% were not referred to catheterization, 20% to 30% were not receiving aspirin, 35% to 44% were not receiving a beta-blocker, and 20% to 25% were not receiving a lipid-lowering agent at 90 days after the index test. Risk-adjusted analyses revealed that compared with stress single-photon emission computed tomography or positron emission tomography, changes in aspirin and lipid-lowering agent use was greater after computed tomography angiography, as was the 90-day catheterization referral rate in the setting of normal/nonobstructive and mildly abnormal test results. CONCLUSIONS: Overall, noninvasive testing had only a modest impact on clinical management of patients referred for clinical testing. Although post-imaging use of cardiac catheterization and medical therapy increased in proportion to the degree of abnormality findings, the frequency of catheterization and medication change suggests possible undertreatment of higher risk patients. Patients were more likely to undergo cardiac catheterization after computed tomography angiography than after single-photon emission computed tomography or positron emission tomography after normal/nonobstructive and mildly abnormal study findings. (Study of Perfusion and Anatomy's Role in Coronary Artery [CAD] [SPARC]; NCT00321399).

Dipyridamole-associated shock and pulmonary edema.

OBJECTIVE: To report a case of fulminant shock and noncardiogenic pulmonary edema induced by intravenously administered dipyridamole. CASE SUMMARY: A 73-year-old woman presented to the office of her cardiologist for dipyridamole myocardial scintigraphy. Several minutes after administration of intravenous dipyridamole 0.57 mg/kg over 4 minutes she developed wheezing, followed by cardiovascular collapse and pulmonary edema requiring 100% oxygen and endotracheal intubation. She had never received dipyridamole before this, and no other medications or exposures were documented proximate to the collapse. On transfer to the hospital, she developed shock refractory to multiple vasopressors, which responded to continuous infusions of epinephrine. She also had severe pulmonary edema requiring invasive ventilation, 100% inspired oxygen, and 24 cm H2O positive end-expiratory pressure. An echocardiogram did not show new left-ventricular dysfunction and there were signs of right-heart underfilling, supporting a diagnosis of noncardiogenic pulmonary edema. Both shock and pulmonary edema resolved within 12 hours. DISCUSSION: Dipyridamole-associated hypotension has been reported in a number of case series and registries. Detailed case descriptions, however, are not available in the literature to permit understanding of the mechanism of shock following hypotension resulting from dipyridamole myocardial scintigraphy. Our case is exceptional in that echocardiography results support a diagnosis of hypovolemic (rather than cardiogenic) shock. To our knowledge, this is the first case of severe (most likely noncardiogenic) pulmonary edema associated with intravenous infusion of dipyridamole. An objective causality assessment suggested that this patient's cardiopulmonary collapse was probably related to dipyridamole. CONCLUSIONS: While hypotension has been previously associated with intravenous use of dipyridamole, ours is the first report to suggest a noncardiogenic mechanism for shock. To our knowledge, this is the first reported case of noncardiogenic pulmonary edema following dipyridamole infusion.

Contribution of mitochondria to cardiac muscle water/macromolecule proton magnetization transfer.

The contribution of mitochondria to water-macromolecule proton magnetization transfer (MT) was evaluated in porcine heart tissue. An examination of isolated mitochondria in suspension, at the same concentration as found in heart tissue, revealed MT effects very similar in magnitude and bandwidth to those in intact heart tissue. Disruption of the gross structure of the mitochondria by freeze-thawing or with detergent resulted in only approximately 25% decreases in MT, which suggests that the structure of the mitochondria is not critical for these effects. The current data indicate that mitochondria macromolecules contribute significantly to MT in the intact heart.

Detecting acute coronary syndrome in the emergency department with cardiac magnetic resonance imaging.

BACKGROUND: Managing chest pain in the emergency department remains a challenge with current diagnostic strategies. We hypothesized that cardiac MRI could accurately identify patients with possible or probable acute coronary syndrome. METHODS AND RESULTS: The diagnostic performance of MRI was evaluated in a prospective study of 161 consecutive patients. Enrollment required 30 minutes of chest pain compatible with myocardial ischemia but an ECG not diagnostic of acute myocardial infarction. MRI was performed at rest within 12 hours of presentation and included perfusion, left ventricular function, and gadolinium-enhanced myocardial infarction detection. MRI was interpreted qualitatively but also analyzed quantitatively. The sensitivity and specificity, respectively, for detecting acute coronary syndrome were 84% and 85% by MRI, 80% and 61% by an abnormal ECG, 16% and 95% for strict ECG criteria for ischemia (ST depression or T-wave inversion), 40% and 97% for peak troponin-I, and 48% and 85% for a TIMI risk score > or =3. The MRI was more sensitive than strict ECG criteria for ischemia (P<0.001), peak troponin-I (P<0.001), and the TIMI risk score (P=0.004), and MRI was more specific than an abnormal ECG (P<0.001). Multivariate logistic regression analysis showed MRI was the strongest predictor of acute coronary syndrome and added diagnostic value over clinical parameters (P<0.001). CONCLUSIONS: Resting cardiac MRI exhibited diagnostic operating characteristics suitable for triage of patients with chest pain in the emergency department. Performed urgently to evaluate chest pain, MRI accurately detected a high fraction of patients with acute coronary syndrome, including patients with enzyme-negative unstable angina.