Pharmacologic intervention for the failing heart has traditionally targeted neurohormonal activation and ventricular remodeling associated with cardiac dysfunction. Despite the multitude of agents available for the treatment of heart failure, it remains a highly prevalent clinical syndrome with substantial morbidity and mortality, necessitating alternative strategies of targeted management. One such area of interest is the ability to modulate myocardial glucose uptake and its impact on cardioprotection. Glucose‐insulin‐potassium (GIK) infusions have been studied for decades, with conflicting results regarding benefit in acute myocardial infarction. Based on the same concepts, glucagon‐like peptide‐1‐[7–36] amide (GLP‐1) has recently been demonstrated to be a more effective alternative in left ventricular (LV) systolic dysfunction. This paper provides a review on the current evidence supporting the use of GLP‐1 in both animal models and humans with ischemic and nonischemic cardiomyopathy. Copyright © 2009 Wiley Periodicals, Inc.

No abstract

Diabetes mellitus is well recognized as a potent and prevalent risk factor for accelerated atherosclerosis and ischemic heart disease. However, there is also evidence of cardiac dysfunction in diabetes in the absence of coronary atherosclerosis, termed diabetic cardiomyopathy. Changes in ventricular structure and left ventricular systolic and diastolic dysfunction have all been noted even in patients with well-controlled diabetes and without overt macrovascular complications. Insulin resistance, hyperglycemia, and increased free fatty acid metabolism promote coronary microvascular disease, sympathetic nervous system dysfunction, and ventricular remodeling, and may contribute to the altered cardiac phenotype seen in diabetes. In addition to standard therapy (angiotensin-converting enzyme inhibitors and beta-blockers), diabetic patients with left ventricular dysfunction are likely to benefit from targeted therapies to reduce insulin resistance and modulate substrate use.

No abstract

Several Boston Scientific pacemaker models have a known issue with intermittent oversensing of the minute ventilation sensor when paired with non-Boston Scientific leads. Several of our patients with these hybrid systems have had transient out of range impedances and oversensing after safety switching which we suspected may be related. A retrospective analysis of 395 patients who had pacemakers implanted between 2015-2017 found that transient out of range impedances with safety switching was present in 9% of Boston Scientific pacemakers paired with Abbott or Medtronic leads compared with 0% in other device-lead combinations (P = 0.0089).We postulate that the root cause of the minute ventilation oversensing and transient high impedance issue is the same, a header-lead interaction from low-level incompatibility. Recognizing this issue is critical to prevent unnecessary lead revisions or extractions as it can be prevented with a simple reprogramming of lead pace/sense configuration.