Single-Center Retrospective Study of Risk Factors and Predictive Value of Framingham Risk Score of Patients with ST Elevation Myocardial Infarction.

OBJECTIVES: The objective of this study was to identify risk factors and clinical profile of the patients presenting with ST elevation myocardial infarction (STEMI). We further evaluated the utility of the Framingham Risk Score (FRS) in the accurate identification of these patients if used before their coronary event. METHODS: We evaluated the demographic, clinical, and angiographic characteristics of patients admitted with STEMI. We also calculated cardiovascular event risk using the FRS in a subset of patients without prior known coronary artery disease and diabetes mellitus. RESULTS: A total of 44 patients, predominantly men (75%) and white (80%), with a mean age of 56 ± 10 years, were included in our analysis. Cigarette smoking was the predominant risk factor (83%) followed by hypertension (77%) and dyslipidemia (68%). The calculated FRS in a subset of patients without prior coronary artery disease or diabetes mellitus was 14.1% ± 5.8%. Based on the FRS, 8 (36%) patients had a 10-year risk >20% and 14 (63%) patients had a 10-year risk between 10% and 20%. CONCLUSIONS: In a series of consecutive patients with STEMI, we observed that high FRS was inadequate in correct identification and risk stratification of the majority of patients who had STEMI. Our study underlines the importance of being familiar with multiple risk scores and choosing the most applicable risk score based on the patient's individual characteristics. In addition, it is important to take into consideration the nontraditional risk factors or measurement of coronary artery calcium as a part of the risk assessment algorithm.

Hematologic markers better predict left ventricular assist device thrombosis than echocardiographic or pump parameters.

BACKGROUND: Left ventricular assist device (LVAD) thrombosis is a life-threatening complication that remains a major clinical problem. Consensus diagnostic criteria do not exist. We investigated whether hematologic, echocardiographic, or pump parameters reliably change during LVAD thrombosis. METHODS: A retrospective analysis of 20 consecutive cases of continuous-flow LVAD thrombosis (Thoratec HeartMate II n = 16, HeartWare HVAD n = 4) was performed. Hematologic markers (lactate dehydrogenase, plasma-free hemoglobin, hemoglobin, creatinine), echocardiographic parameters (left ventricular end-systolic and end-diastolic diameter, mitral regurgitation, aortic insufficiency, inflow-cannula velocity), and pump characteristics (speed, power, estimated flow, pulsatility index) were analyzed with one-way repeated measures ANOVA with Tukey post-test or paired Student t-tests. RESULTS: Lactate dehydrogenase and plasma-free hemoglobin were significantly (p < 0.05) elevated at admission for LVAD thrombosis. Hemoglobin and creatinine were not significantly different at admission but changed significantly after admission. Left ventricular end-systolic and end-diastolic diameter, mitral regurgitation, aortic insufficiency, inflow-cannula velocity, LVAD speed, power consumption, estimated flow, and pulsatility index were not significantly different at admission for LVAD thrombosis. CONCLUSION: Hematological markers of hemolysis, but not echocardiographic or pump parameters, reliably changed during LVAD thrombosis. Markers of hemolysis are the best early predictors of LVAD thrombosis.

Vitamin D reduces left atrial volume in patients with left ventricular hypertrophy and chronic kidney disease.

BACKGROUND: Left atrial enlargement, a sensitive integrator of left ventricular diastolic function, is associated with increased cardiovascular morbidity and mortality. Vitamin D is linked to lower cardiovascular morbidity, possibly modifying cardiac structure and function; however, firm evidence is lacking. We assessed the effect of an activated vitamin D analog on left atrial volume index (LAVi) in a post hoc analysis of the PRIMO trial (clinicaltrials.gov: NCT00497146). METHODS AND RESULTS: One hundred ninety-six patients with chronic kidney disease (estimated glomerular filtration rate 15-60 mL/min per 1.73 m(2)), mild to moderate left ventricular hypertrophy, and preserved ejection fraction were randomly assigned to 2 µg of oral paricalcitol or matching placebo for 48 weeks. Two-dimensional echocardiography was obtained at baseline and at 24 and 48 weeks after initiation of therapy. Over the study period, there was a significant decrease in LAVi (-2.79 mL/m(2), 95% CI -4.00 to -1.59 mL/m(2)) in the paricalcitol group compared with the placebo group (-0.70 mL/m(2) [95% CI -1.93 to 0.53 mL/m(2)], P = .002). Paricalcitol also attenuated the rise in levels of brain natriuretic peptide (10.8% in paricalcitol vs 21.3% in placebo, P = .02). For the entire population, the change in brain natriuretic peptide correlated with change in LAVi (r = 0.17, P = .03). CONCLUSIONS: Forty-eight weeks of therapy with an active vitamin D analog reduces LAVi and attenuates the rise of BNP. In a population where only few therapies alter cardiovascular related morbidity and mortality, these post hoc results warrant further confirmation.

Vitamin D therapy and cardiac structure and function in patients with chronic kidney disease: the PRIMO randomized controlled trial.

CONTEXT: Vitamin D is associated with decreased cardiovascular-related morbidity and mortality, possibly by modifying cardiac structure and function, yet firm evidence for either remains lacking. OBJECTIVE: To determine the effects of an active vitamin D compound, paricalcitol, on left ventricular mass over 48 weeks in patients with an estimated glomerular filtration rate of 15 to 60 mL/min/1.73 m(2). DESIGN, SETTING, AND PARTICIPANTS: Multinational, double-blind, randomized placebo-controlled trial among 227 patients with chronic kidney disease, mild to moderate left ventricular hypertrophy, and preserved left ventricular ejection fraction, conducted in 11 countries from July 2008 through September 2010. INTERVENTION: Participants were randomly assigned to receive oral paricalcitol, 2 µg/d (n =115), or matching placebo (n = 112). MAIN OUTCOME MEASURES: Change in left ventricular mass index over 48 weeks by cardiovascular magnetic resonance imaging. Secondary end points included echocardiographic changes in left ventricular diastolic function. RESULTS: Treatment with paricalcitol reduced parathyroid hormone levels within 4 weeks and maintained levels within the normal range throughout the study duration. At 48 weeks, the change in left ventricular mass index did not differ between treatment groups (paricalcitol group, 0.34 g/m(2.7) [95% CI, -0.14 to 0.83 g/m(2.7)] vs placebo group, -0.07 g/m(2.7) [95% CI, -0.55 to 0.42 g/m(2.7)]). Doppler measures of diastolic function including peak early diastolic lateral mitral annular tissue velocity (paricalcitol group, -0.01 cm/s [95% CI, -0.63 to 0.60 cm/s] vs placebo group, -0.30 cm/s [95% CI, -0.93 to 0.34 cm/s]) also did not differ. Episodes of hypercalcemia were more frequent in the paricalcitol group compared with the placebo group. CONCLUSION: Forty-eight week therapy with paricalcitol did not alter left ventricular mass index or improve certain measures of diastolic dysfunction in patients with chronic kidney disease. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT00497146.

Vitamin D receptor activation and left ventricular hypertrophy in advanced kidney disease.

BACKGROUND: In chronic kidney disease (CKD), left ventricular hypertrophy (LVH) is prevalent and is associated with increased cardiovascular morbidity and mortality. Vitamin D receptor (VDR) activation attenuates LVH progression in animal models. METHODS: PRIMO is a multinational, randomized, double-blinded trial with oral paricalcitol in subjects with stages 3-4 CKD, mild-to-moderate LVH and an LV ejection fraction >50%. The primary endpoint is change in the left ventricular mass index (LVMI) compared with placebo after 48 weeks of treatment. The main secondary endpoints are changes in diastolic function parameters. In this paper, we report baseline characteristics from this study. RESULTS: LVMI was 33.0 ± 7.5 g/m(2.7) for males and 30.8 ± 7.2 g/m(2.7) for females (p = 0.04). LVMI correlated with systolic blood pressure (r = 0.24), urine albumin creatinine ratio (r = 0.39), troponin T (r = 0.29), high-sensitivity C-reactive protein (r = 0.25) and plasma levels of B-type brain natriuretic peptide (r = 0.22); all p < 0.01. In multiple linear regression, each remained independently associated with LVMI. The early diastolic velocity of the lateral mitral annulus (E') was 8.1 ± 2.4 cm/s. E' was inversely correlated with age in univariate (r = -0.14, p = 0.04) and multivariable (p = 0.02) analysis. CONCLUSION: Among 227 multinational subjects with stages 3-4 CKD, baseline LVMI correlates with baseline blood pressure, urine albumin creatinine ratio and cardiac biomarkers, and baseline diastolic function correlates with age. This research was funded by Abbott Laboratories; ClinicalTrials.gov No. NCT00497146.

Rapid Extracorporeal Membrane Oxygenation Overcomes Fulminant Myocarditis Induced by 5­Fluorouracil.

Fulminant myocarditis is a rare but potentially life-threatening illness caused by 5-fluorouracil cardiotoxicity. Data supporting the use of extracorporeal membrane oxygenation for the treatment of fulminant myocarditis are limited. A 49-year-old, previously healthy white man, recently diagnosed with anal squamous cell carcinoma, developed severe chest pain hours after completing his first 96-hour intravenous 5-fluorouracil treatment. Over a period of 3 days from onset of symptoms, the patient developed cardiogenic shock secondary to fulminant myocarditis induced by 5-fluorouracil cardiotoxicity. This required emergency initiation of extracorporeal membrane oxygenation. The patient's systolic function recovered by day 5, and on the 17th day he was discharged in hemodynamically stable condition, without symptoms of heart failure. This case shows the importance of prompt recognition of cardiogenic shock secondary to 5-fluorouracil-induced myocarditis and how the immediate initiation of extracorporeal membrane oxygenation can restore adequate tissue perfusion, leading to myocardial recovery and ultimately the survival of the patient.

Diagnostic dilemma: Takotsubo cardiomyopathy versus acute coronary syndrome.

Takotsubo cardiomyopathy is a kind of non-ischemic cardiomyopathy characterized by transient apical ballooning of the heart. This often results from sudden, temporary weakening of the myocardium. Initially defined in the absence of coronary artery disease, it has since expanded to involve patients with coronary artery disease. This inclusion is not free of challenges now faced at distinguishing between the two when they occur concomitantly, impacting the therapeutic interventions. We present a case of takotsubo cardiomyopathy with simultaneous coronary artery disease that responded well to conservative management and resulted in complete recovery of the patient. This reiterates the principle that a case-by-case evaluation of patients with takotsubo cardiomyopathy with underlying coronary artery disease needs to be made before an individualized therapeutic approach can be taken.

Statin therapy in the reduction of cardiovascular events in patients undergoing intermediate-risk noncardiac, nonvascular surgery.

BACKGROUND: Hydroxymethylglutaryl-coenzyme A reductase inhibitors (statins) reduce perioperative cardiac events in high-risk patients undergoing cardiovascular surgery. However, there is paucity of data on the role of statins in patients undergoing intermediate-risk noncardiac, nonvascular surgery (NCNVS). HYPOTHESIS: Statins are cardioprotective in intermediate-risk NCNVS. METHODS: We identified a retrospective cohort of patients undergoing intermediate risk NCNVS. Our composite end point (CEP) included 30-day all-cause mortality, atrial fibrillation (AF), and nonfatal myocardial infarction (MI). A stepwise logistic regression with adjustment using propensity scores was performed to determine if statin therapy was independently associated with the risk reduction of adverse postoperative cardiovascular outcomes. RESULTS: We identified 752 patients. Seventy-five of them (9.97%) developed composite end points; 10 (1.33%) had in-hospital nonfatal MI, 44 (5.85%) developed AF, and 35 (4.65%) died within 30 days. The 30-day all-cause mortality was 31/478 (6.48%) among statin nonusers vs 4/274 (1.45%) for statin users (P < 0.002). As compared with nonusers, patients on statin therapy had a 5-fold reduced risk of 30-day all-cause mortality. Statin therapy was associated with decreased CEP after adjusting for baseline characteristics, with a propensity score to predict use of statins (odds ratio [OR]: 0.54, 95% confidence interval [CI]: 0.30-0.97, P = 0.039). After further adjustment for propensity score, diabetes mellitus, percutaneous coronary intervention, and prior coronary artery bypass grafting, statin therapy proved beneficial (OR: 0.51, 95% CI: 0.28-0.92, P = 0.026). CONCLUSIONS: Statin use in the perioperative period was associated with a reduction in cardiovascular adverse events and 30-day all-cause mortality in patients undergoing intermediate-risk NCNVS.

Amiodarone - a 'broad spectrum' antiarrhythmic drug.

Amiodarone, an iodinated benzofuran derivative, introduced in 1960's as an anti-anginal agent, emerged as a potent anti-arrhythmic agent by 1970's and is currently one of the most commonly prescribed drugs in US for ventricular and atrial arrhythmias. Although amiodarone is considered a class III anti-arrhythmic agent, it also has class I, II, IV actions, making it a unique and effective anti-arrhythmic agent. Because of its minimal negative inotropic activity and very low rate of pro-arrhythmia, it is considered safe in treating arrhythmias in patients with Coronary Artery Disease and Left ventricular systolic dysfunction. Despite these advantages, long term oral therapy with amiodarone is limited by side effect profile involving various organs like thyroid, lung, heart, liver, skin etc. Though the side effects can be decreased significantly by keeping the maintenance dose at 200 to 300 mg/day, patients on amiodarone should be followed closely. Amiodarone interacts with medications such as Warfarin, Digoxin, Macrolides, Floroquinolones etc., which share Cytochrome P450 metabolic pathway. Hence reducing their doses prior to starting amiodarone is recommended. Amiodarone, a category D drug, is contraindicated in pregnant and breast feeding women. This review discusses the pharmacokinetics of amiodarone, its evolving clinical indications, management of toxicity and drug interactions.