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Introduction: Statin therapy is potentially the most important treatment presently available to prevent the progression of atherosclerosis. Unfortunately, a significant number of patients cannot tolerate statins due to muscle aches. Vitamin D deficiency, which is also associated with a variety of muscular symptoms, is commonly identified among patients with an indication for statin therapy. Several small studies have proposed that vitamin D deficiency may contribute to statin intolerance, but this has not been definitively demonstrated. Hypothesis: Vitamin D deficiency is associated with greater risk of statin intolerance. Methods: In the Intermountain Healthcare electronic health record, 12,066 patients had an initial 25(OH) vitamin D (VitD) level available and an indication for statin therapy with either a documented statin intolerance or evidence of active statin therapy. Patient baseline clinical characteristics were collected and multivariable logistic regression analysis was used to evaluate associations between VitD levels (stratified into four categories (ng/ml): Results: Overall, 12,066 subjects (statin intolerant n=928 [7.7%]; age = 56±6 yrs; males = 37.5%, prior atherosclerotic cardiovascular disease = 1856 [15.4%]) were enrolled. Multivariable effects of VitD and other predictors on risk of statin intolerance are shown in the Table. Conclusion: In this large cohort of patients with an indication for statin therapy, baseline VitD levels were not significantly associated with statin intolerance. Characteristics that were associated with statin intolerance included older age, female gender, Caucasian race, diabetes and a prior diagnosis of hyperlipidemia.

Background: Randomized trials report that prolonged (>1 year) use of P2Y12 inhibitors with aspirin after myocardial infarction (MI) reduces stent thrombosis and cardiovascular (CV) events, including new MI, stroke, and CV death. Post-MI patients may benefit to a differing extent from long-term dual anti-platelet therapy (DAPT); thus, a method is needed to identify those at higher risk of CV events. Hypothesis: A low-cost, easy-to-use, and highly predictive risk stratification tool can be created to differentiate risk of CV events 1-3 years after MI. Methods: Patients surviving ≥1 year after an index MI who had ≥1 additional risk factor for MI were studied. Cox regression models were used to derive sex-specific Intermountain Acute Coronary Syndromes (IMACS) risk scores in 70% of patients (N=1,342 females; 3,047 males). Validation of IMACS scores was performed in the other 30% of patients (N=576 females; 1,290 males). Variables used in model creation were age, troponin I, B-type natriuretic peptide, hemoglobin A1c, and all components of the lipid panel, complete blood count, and comprehensive metabolic panel. The primary end point was a composite of CV death, MI, or stroke. Results: Age averaged 68.7±12 and 69.8±12 for females in the derivation and validation groups, respectively, and 63.6±12 and 63.9±12 for males. IMACS scores ranged from 0-11 for females (grouping scores of 0-2, 3-6, and 7-11 into low-, moderate-, and high-risk) and 0-14 for males (0-2, 3-7, 8-14). In the validation groups, IMACS categories stratified CV event risk (Figure). IMACS c-statistics for females were c=0.675 and c=0.734 in derivation and validation groups, respectively, and for males c=0.715 and c=0.672. Conclusion: Sex-specific IMACS risk scores strongly stratified 1- to 3-year post-MI risk of CV events. IMACS is an inexpensive electronic health record tool that empowers the evaluation of which post-MI patients may be the best candidates for more aggressive therapeutic management.

Introduction: Diabetes mellitus (DM) is associated with poor cardiovascular disease (CVD) outcomes, especially in the setting of acute myocardial infarction (AMI). As both a first diagnosis (dx) of DM and missed dx of incident DM also may be associated with poor outcomes; we sought to determine their frequency and related CVD impact in patients presenting with AMI. Hypothesis: Many individuals with AMI have undiagnosed DM based on standard criteria, which leads to poor MACE outcomes. Methods: Patients (pts) presenting with AMI between 2002 and 2013 were studied (n=5719). Criteria-defined (CD)-DM was a fasting glucose (FG) ≥126 mg/dL, a random glucose (RG) ≥200, or a hemoglobin A1c ≥6.5%. DM groups were: 1) history (hx) of DM (n=1941, 34%), 2) no hx of DM, with CD-DM undiagnosed at AMI (n=500, 9%), 3) no hx of DM, with CD-DM diagnosed (dx) at hospitalization (n=207, 4%), and 4) no hx of DM and no CD-DM (n=3071, 53%). MACE (all-cause death, MI, stroke, heart failure hospitalization) was determined at 1 year post discharge. Results: Univariate comparisons are shown in the Table. After adjusting for covariables in a multivariate logistic regression using subjects with no hx of DM as the referent, hx of DM (OR=1.6; 95% CI: 1.3, 2.0; p Conclusions: The prevalence of DM is high in those presenting with AMI. Recognition of undiagnosed DM in the setting of CD-DM remains poor. Furthermore, MACE outcomes are 1.5 times higher with CD-DM undiagnosed than without DM, whereas outcomes are moderated if CD-DM is recognized at the time of AMI. Protocols for more aggressive identification of incident DM should be instituted and may importantly impact clinical outcomes for pts with previously undiagnosed DM.

Introduction: Epidemiologic studies have identified low testosterone (T) levels as an independent risk factor for cardiovascular (CV) and total mortality. However, the impact of T therapy on CV outcomes is controversial. A small trial in older men at high risk was stopped early due to increased CV events (NEJM 2010; 363:109). A recent observational study in veterans suggested modest risk (JAMA 2013; 3310:1829). We sought to assess the impact of T supplementation and achieved T levels across Intermountain Healthcare (IHC) facilities using a virtual controlled study design. Methods: IHC electronic medical records were searched between 1996 and 2011 to identify subjects who had a low initial total T level, a subsequent T level, and ≤3y follow-up. Levels were correlated with T supplement use. Primary outcomes were a composite of death, nonfatal myocardial infarction, and stroke (MACE) and death alone (D). Hazard ratios (HRs) comparing groups of persistent low (742 ng/dL, n=1919) achieved T were calculated by Cox regression, adjusting for 17 baseline variables. Results: A total of 5,695 men (age 62.3 ± 9.3 y, diabetes: 28%, CAD: 22%) were studied. Event rates at 1 and 3-y by T level, and adjusted HRs, are shown in the Table. Overall 3-y rates of MACE and D were 8.6% and 6.4%, respectively. Subjects supplemented to normal/high T had reduced 3-y MACE (HR 0.55, 95% CI 0.46-0.67) and D (HR 0.43, CI 0.35-0.54) compared to persistent low T subjects, with no signal for effect attenuation for MACE or D with higher T. Results were similar for 1-y MACE (HR 0.51, p Conclusions: In a large general healthcare population, T therapy in men with low T was associated with reduced MACE and D over 3-y compared to no or ineffective supplementation. Resolving the difference in CV risk impact of T therapy between this, and previous studies, warrants a large randomized clinical trial in a similar, younger population.

Introduction: Epidemiologic studies have identified high LDL cholesterol levels as an independent risk factor for cardiovascular (CV) disease, and randomized trials with statin therapy have demonstrated added clinical benefit when LDL levels are reduced to at least 70 mg/dL. However, whether targeting significantly lower secondary prevention LDL levels is beneficial, or perhaps actually may be unsafe, is not known. Methods: Patients undergoing coronary angiography who were documented to have significant (≥50% stenosis) coronary artery disease (CAD), discharged on statin therapy with an LDL level Results: A total of 5,222 patients (age = 66±12 yrs, men = 72%, hypertension = 69%, diabetes = 30%, smokers = 29%, ACS presentation = 69%) were studied. Follow-up for the ultra low, very low and low LDL categories was 6.1±4.3, 6.4±3.9 and 7.3±4.1 yrs respectively. Event rates and adjusted HRs are shown in the Table. Conclusions: In a large secondary prevention population with significant CAD on statin therapy, treating LDL cholesterol levels to

Background— Coronary artery bypass surgery (CABG) and percutaneous coronary intervention with stenting (PCI-S) are both safe and effective approaches for revascularization in patients with multivessel coronary artery disease. However, conflicting information exists when comparing the efficacy of the two methods. In this study, we examined the outcomes of major adverse cardiovascular events and death for subgroups of typical “real-world” patients undergoing coronary revascularization in the modern era. Methods and Results— Patients were included if they were revascularized by CABG or PCI-S, had ≥5 years of follow-up, and had ≥2-vessel disease. Patients were followed for an average of 7.0±3.2 years for incidence of death and major adverse cardiovascular events (death, myocardial infarction, or repeat revascularization). Multivariate regression models were used to correct for standard cardiac risk factors including age, sex, hyperlipidemia, diabetes mellitus, family history of coronary artery disease, smoking, hypertension, heart failure, and renal failure. Subgroup analyses were also performed, stratified by age, sex, diabetes, ejection fraction, and history of PCI-S, CABG, or myocardial infarction. A total of 6369 patients (CABG 4581; PCI-S 1788) were included. Age averaged 66±10.9 years, 76% were male, and 26% were diabetic. Multivariate risk favored CABG over PCI-S for both death (hazard ratio 0.85; P =0.001) and major adverse cardiovascular events (hazard ratio 0.51; P Conclusions— In this large observational study of patients undergoing revascularization for multivessel coronary artery disease, a long-term benefit was found, in relationship to both death and major adverse cardiovascular events, for CABG over PCI-S regardless of diabetic status or other stratifications.

Enoxaparin has become an attractive therapy for use during acute coronary syndrome (ACS) because of its potential superior efficacy over unfractionated heparin (UFH), its longer activity, and its subcutaneous route of administration. However, because a significant number of patients presenting with ACS may be sent directly to open heart surgery while still on anticoagulation, it is important to understand any potential bleeding risks that may be associated with the use of enoxaparin under these circumstances.From 1998 to 2001, 1159 consecutive patients presenting with an acute coronary syndrome who received either UFH (n=1008) or enoxaparin (n=151) before proceeding to open heart surgery for urgent therapy during the same hospitalization were included in this study. Incidence of perioperative bleeding as evidenced by the units of blood products (packed red blood cells or platelets) transfused or the need for surgical re-exploration for postoperative bleeding was recorded.Average age was 65+/-11 and 67+/-11 years for patients receiving UFH and enoxaparin, respectively (P=0.005). Seventy-five percent of those receiving UFH and 64% of those receiving enoxaparin (P0.005) were males. After discharge, the incidence of rehospitalization for hemorrhage requiring return to surgery for re-exploration was 7.9% in the enoxaparin group and 3.7% in the UFH group (adjusted hazard ratio=2.6, P=0.03). The use of blood products did not differ between groups (UFH=2.7+/-6.5 U and enoxaparin=2.3+/-4.5 U; P=NS).The preoperative use of enoxaparin compared with UFH in patients presenting with an ACS who undergo open-heart surgery during the same hospitalization is associated with a significantly increased incidence of re-exploration for postoperative bleeding. Further study is needed to understand the mechanism of this phenomenon and to develop appropriate guidelines to address this potentially important issue.

Background Enoxaparin has become an attractive therapy for use during acute coronary syndrome (ACS) because of its potential superior efficacy over unfractionated heparin (UFH), its longer activity, and its subcutaneous route of administration. However, because a significant number of patients presenting with ACS may be sent directly to open heart surgery while still on anticoagulation, it is important to understand any potential bleeding risks that may be associated with the use of enoxaparin under these circumstances. Methods From 1998 to 2001, 1159 consecutive patients presenting with an acute coronary syndrome who received either UFH (n=1008) or enoxaparin (n=151) before proceeding to open heart surgery for urgent therapy during the same hospitalization were included in this study. Incidence of perioperative bleeding as evidenced by the units of blood products (packed red blood cells or platelets) transfused or the need for surgical re-exploration for postoperative bleeding was recorded. Results Average age was 65±11 and 67±11 years for patients receiving UFH and enoxaparin, respectively ( P= 0.005). Seventy-five percent of those receiving UFH and 64% of those receiving enoxaparin ( P P =0.03). The use of blood products did not differ between groups (UFH=2.7±6.5 U and enoxaparin=2.3±4.5 U; P =NS). Conclusion The preoperative use of enoxaparin compared with UFH in patients presenting with an ACS who undergo open-heart surgery during the same hospitalization is associated with a significantly increased incidence of re-exploration for postoperative bleeding. Further study is needed to understand the mechanism of this phenomenon and to develop appropriate guidelines to address this potentially important issue.

Ventricular function was evaluated in 18 patients prior to left ventriculography and selective coronary arteriography. Simultaneous left ventricular pressure (catheter-tip manometer) and dP/dt were recorded at resting heart rates and during tachycardia induced by right atrial pacing. Pressure-velocity curves were constructed from which V max and maximum measured contractile element velocity (max V CE ) were obtained. V max and max V CE initially increased with pacing-induced tachycardia in 17 of the 18 patients. Eight patients developed evidence of myocardial ischemia during atrial pacing. During the period of myocardial ischemia there was a decrease in V max and max V CE in all eight patients despite constant or increasing heart rate. In the 10 patients who did not develop evidence of myocardial ischemia with pacing-induced tachycardia, V max and max V CE continued to increase or remained constant with increasing rate. Peak left ventricular dP/dt increased coincident with the onset of myocardial ischemia in six of eight patients despite a fall in V max and max V CE in all eight patients during the ischemic period. A highly significant difference was demonstrated between V max values of patients with normal ejection fractions and patients with low ejection fractions, both at rest and during pacing-induced tachycardia.

This report describes a 52-year-old black male with the isolated finding of an anomalous superior vena cava draining into the left atrium. The patient presented with dizziness, mild cyanosis, polycythemia and normal cardiac and pulmonary findings. The first major diagnostic clue in this confusing clinical presentation was an unsuccessful lung perfusion scan in which intravenous tracer consistently bypassed the lungs. This appears to be the first adult presenting with this rare anomaly. This condition should be suspected if cyanosis, clubbing, and a "normal" cardiac examination coexist and if the more common pulmonary and hematological causes of this triad have been excluded.