A significant proportion of diabetic CAD patients fail to achieve pre-specified targets for 4 major modifiable cardiovascular risk factors in clinical trials. We conclude that fundamentally new thinking is needed to explore approaches to achieve optimal secondary prevention treatment goals. (Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation; NCT00007657) (Bypass Angioplasty Revascularization Investigation 2 Diabetes [BARI 2D]; NCT00006305) (Comparison of Two Treatments for Multivessel Coronary Artery Disease in Individuals With Diabetes [FREEDOM]; NCT00086450).

The prevalence of Type 2 diabetes mellitus (DM) continues to increase globally and brings with it a parallel increase in the associated cardiovascular disease complications. Despite advances in evidence-based therapies for cardiovascular disease risk modification, many of which are especially effective among patients with DM, there remains a residual degree of cardiovascular disease risk associated with DM, yielding opportunity for continued clinical advances. Given the myriad perturbations of platelet function associated with DM, improvements in antiplatelet therapies hold particular promise for this high-risk population of patients, with emerging data from ex vivo assessments and clinical outcomes trials providing a basis of support for this concept.

Type 2 diabetes mellitus (DM) is associated with increased risk for developing heart failure (HF) and worse outcomes once HF is present. While the exact mechanisms underpinning these observations remain poorly understood, several metabolic perturbations associated with DM have been implicated as contributors to the HF risk, including alterations of cardiomyocyte metabolic substrate switching between free fatty acid (FFA) and glucose metabolism; increased FFA exposure and cellular accumulation; and alterations in peroxisome proliferator-activated receptor-(PPAR-)alpha activity, among others. The commonly coincident conditions of left ventricular hypertrophy and ischemic heart disease likely confound the metabolic derangements further increasing HF risk. Continued investigation into these mechanistic connections is necessary to better understand the pathophysiology and ideally inform the pursuit of novel therapeutic targets and strategies to intervene on the HF associated with DM.

DES is a safe and effective long-term option for CLI due to severe infrapopliteal arterial disease. Long-term vascular patency led to a high rate of limb preservation and low amputation rate. A multicenter trial should further elucidate the role of DES in the treatment of CLI.

Left ventricular pseudoaneurysms that develop in the setting of infective endocarditis are believed to result from remodeling of extravalvular abscesses. The high pressure generated by the left ventricle is thought to dissect into the abscess causing it to form a characteristic sac-like protuberance readily recognized echocardiographically. Left ventricular pseudoaneurysms most often arise from abscesses in the mitral-aortic intervalvular fibrosa and protrude external to the aorta. Less often, as described herein, they arise from abscesses external the posterior mitral annulus and project into the posterior interventricular groove. Perforation may result in camo-cameral or aorto-cameral fistula formation, as well as fistulous communication with the pericardial space.