The Cardiac Microvasculature in Hypertension, Cardiac Hypertrophy and Diastolic Heart Failure

Abstract

Recent studies revealed an exceedingly high mortality with diastolic heart failure that was previously regarded as relatively benign compared to systolic heart failure. Prominent risk factors for diastolic heart failure are increasing age, hypertension and diabetes. These risk factors are associated with coronary microvascular rarefaction and resultant decreased coronary flow reserve, thereby rendering the myocardium vulnerable to ischemia. We discuss the importance of angiogenic gene programming in preserving the coronary microvasculature, preserving cardiac function and altering disease course. Further, we discuss the possible utility of therapies that activate hypoxia inducible factor-1 in preventing rarefaction of the coronary microvasculature and maintaining cardiac diastolic function.

PET imaging of cardiac hypoxia: Opportunities and challenges

“…Pathologic cardiac hypertrophy is central to this pathophysiology because the lack of proportionate microvascular growth leaves the myocardium vulnerable to ischemia [27]. In this context, ischemia and hypoxia contribute to the pathophysiology of heart failure, but since its clinical presentation is typically less dramatic and more diffuse than acute myocardial infarction, and can occur in the absence of coronary artery disease, our inability to detect it means that we are missing an important opportunity to intervene.…”

“…In this context, ischemia and hypoxia contribute to the pathophysiology of heart failure, but since its clinical presentation is typically less dramatic and more diffuse than acute myocardial infarction, and can occur in the absence of coronary artery disease, our inability to detect it means that we are missing an important opportunity to intervene. This decreased vascularity in hypertrophic myocardium is exacerbated by increases in myocyte size and tissue fibrosis, which increase diffusion distances and decrease oxygen availability to myocytes (and perhaps more importantly, their mitochondria) [27,28]. While up-regulation of hypoxia inducible factor HIF-1α is increasingly being recognized as an important instigator of cardiac hypertrophy [29][30][31] and mediator of decline into heart failure [32][33][34], we have found no reports that successfully demonstrate non-invasive measurement of hypoxia itself in hypertrophic or failing myocardium.…”

Use of cereal bars with quinoa (Chenopodium quinoa W.) to reduce risk factors related to cardiovascular diseases

“…Therefore, recently, there has been a search for alternatives that are easier to obtain and can act as supporting factors in the treatment of the risk indicators, such as obesity, dyslipidemia, and high blood pressure. As a result, dietary alterations associated with economic, social and demographic changes and their effects on human health have been observed in several developing countries (HOENIG et al, 2008). The increasing substitution of fresh foods rich in fibers, vitamins, and minerals for industrialized products, allied to a sedentary lifestyle favored by changes in the work structure and technological advances, represents one of the major etiological factors in obesity associated with systemic arterial hypertension, dyslipidemias, cardiovascular diseases and metabolic syndrome.…”

64Cu-CTS: A Promising Radiopharmaceutical for the Identification of Low-Grade Cardiac Hypoxia by PET

“…31 P MR spectra were acquired on an Avance III 9.4T spectrometer (Bruker) using a 15-mm 31 P/ 1 H birdcage coil (20). Shimming was performed on the 1 H line shape of water (full width at half maximum, ,20 Hz).…”

“…Methods: Rat hearts were perfused with aerobic buffer for 20 min, followed by a range of hypoxic buffers (using a computer-controlled gas mixer) for 45 min. Contractility was monitored by intraventricular balloon, energetics by 31 P nuclear MR spectroscopy, lactate and creatine kinase release spectrophotometrically, and hypoxia-inducible factor 1-α by Western blotting. Results: We identified a key hypoxia threshold at a 30% buffer O 2 saturation that induces a stable and potentially survivable functional and energetic compromise: left ventricular developed pressure was depressed by 20%, and cardiac phosphocreatine was depleted by 65.5% ± 14% (P , 0.05 vs. control), but adenosine triphosphate levels were maintained.…”