Clinica Chimica Acta Volume 412, Issues 17–18, 17 August 2011, Pages 1493–1514

Diet is a key modifiable risk factor in the prevention and risk reduction of coronary heart disease (CHD). Results from the Seven Countries Study in the early 1970s spurred an interest in the role of single nutrients such as total fat in CHD risk. With accumulating evidence, we have moved away from a focus on total fat to the importance of considering the quality of fat. Recent meta-analyses of intervention studies confirm the beneficial effects of replacing saturated fat with polyunsaturated fatty acids on CHD risk. Scientific evidence for a detrimental role of trans fat intake from industrial sources on CHD risk has led to important policy changes including listing trans fatty acid content on the “Nutrition Facts” panel and banning the use of trans fatty acids in food service establishments in some cities. The effects of such policy changes on changes in CHD incidence are yet to be evaluated. There has been a surging interest in the protective effects of vitamin D in primary prevention. Yet, its associations with secondary events have been mixed and intervention studies are needed to clarify its role in CHD prevention. Epidemiological and clinical trial evidence surrounding the benefit of B vitamins and antioxidants such as carotenoids, vitamin E, and vitamin C, have been contradictory. While pharmacological supplementation of these vitamins in populations with existing CHD has been ineffective and, in some cases, even detrimental, data repeatedly show that consumption of a healthy dietary pattern has considerable cardioprotective effects for primary prevention. Results from these studies and the general ineffectiveness of nutrient-based interventions have shifted interest to the role of foods in CHD risk reduction. The strongest and most consistent protective associations are seen with fruit and vegetables, fish, and whole grains. Epidemiological and clinical trial data also show risk reduction with moderate alcohol consumption. In the past decade, there has been a paradigm shift in nutritional epidemiology to examine associations between dietary patterns and health. Several epidemiological studies show that people following the Mediterranean style diet or the Dietary Approaches to Stop Hypertension (DASH) diet have lower risk of CHD and lower likelihood of developing hypertension. Studies using empirical or data driven dietary patterns have frequently identified two patterns — “Healthy or Prudent” and “Western”. In general, the “Healthy”, compared to the “Western” pattern has been associated with more favorable biological profiles, slower progression of atherosclerosis, and reduced incidence. Evidence on changes in dietary patterns and changes in CHD risk is still emerging. With the emergence of the concept of personalized nutrition, studies are increasingly considering the role of genetic factors in the modulation of the association between nutrients and CHD. More studies of genetic variation and dietary patterns in relation to CHD are needed.

CMAJ 2005;173(10):1191-202

It has been known for 50 years that transaminase activity increases in patients with acute myocardial infarction. With the development of creatine kinase (CK), biomarkers of cardiac injury began to take a major role in the diagnosis and management of patients with acute cardiovascular disease. In 2000 the European Society of Cardiology and the American College of Cardiology recognized the pivotal role of biomarkers and made elevations in their levels the “cornerstone” of diagnosis of acute myocardial infarction. At that time, they also acknowledged that cardiac troponin I and T had supplanted CK-MB as the analytes of choice for diagnosis. In this review, we discuss the science underlying the use of troponin biomarkers, how to interpret troponin values properly and how to apply these measurements to patients who present with possible cardiovascular disease.

Heart and Metabolism no:32 2006

Substantial changes in cardiac energy metabolism have been observed in a variety of heart diseases. Understanding the functional role of these changes is critical for developing the concept of metabolic intervention for heart disease. The use of genetically engineered mice in recent studies has made it possible to alter cardiac metabolism independently of secondary influence by disease and, thus, allow the causal role of metabolic remodeling in the pathogenesis and progression of heart disease – in particular, heart failure – to be tested. Results from these studies also shed light on the potential tactics for targeting energy metabolism in heart failure.

J Clin Invest. 2005 Mar;115(3):547-55.

“Oxidation of fatty acids (FAs) and glucose in mitochondria accounts for the vast majority of ATP generation in the healthy adult heart. FAs are the preferred substrate in the adult myocardium, supplying about 70% of total ATP. FAs derived from circulating triglyceride-rich lipoproteins and albumin-bound nonesterified FAs are oxidized in the mitochondrial matrix by the process of FA beta-oxidation (FAO), whereas pyruvate derived from glucose and lactate is oxidized by the pyruvate-dehydrogenase (PDH) complex, localized within the inner mitochondrial membrane. Acetyl-CoA, derived from both pathways, enters the tricarboxylic acid (TCA) cycle. Reduced flavin adenine dinucleotide (FADH2) and NADH are generated via substrate flux through the beta-oxidation spiral and the TCA cycle, respectively. The reducing equivalents enter the electron transport chain, producing an electrochemical gradient across the mitochondrial membrane that drives ATP synthesis in the presence of molecular oxygen (oxidative phosphorylation).”

Figure 1
Pathways involved in cardiac energy metabolism. FA and glucose oxidation are the main ATP-generating pathways in the adult mammalian heart. Acetyl-CoA derived from FA and glucose oxidation is further oxidized in the TCA cycle to generate NADH and FADH2, which enter the electron transport/oxidative phosphorylation pathway and drive ATP synthesis. Genes encoding enzymes involved at multiple steps of these metabolic pathways (i.e., uptake, esterification, mitochondrial transport,and oxidation) are transcriptionally regulated by PGC-1α with its nuclear receptor partners, including PPARs and ERRs (blue text). Glucose uptake/oxidation and electron transport/oxidative phosphorylation pathways are also regulated by PGC-1α via other transcription factors, such as MEF-2 and NRF-1. Cyt c, cytochrome c.

Figure 3
Cardiac energy substrate selection is a dynamic balance influenced by developmental, physiological, and pathological cues. In the fetal heart, glucose oxidation is favored, whereas FA oxidation serves as the major ATP-generating pathway in the adult myocardium. Significant shifts in substrate preference occur in response to dietary (insulin) and physiological (exercise) stimuli. Certain pathophysiological contexts, such as hypertrophy and ischemia, drive metabolism toward glucose utilization, whereas in uncontrolled diabetes, the heart utilizes FAs almost exclusively. In some cases, as in early response to pressure overload–induced hypertrophy, these metabolic shifts are thought to be protective. Alterations in activity or expression of nuclear receptors (PPARs and ERRs) and PGC-1α mediate these shifts in energy substrate utilization.