The Heart In Diabetes Mellitus Biology Essay

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A substantial morbidity and mortality in the population is due to cardiovascular diseases. Atherosclerotic coronary artery disease is responsible for cardiac manifestations in the majority of diabetic patients. Coronary heart disease is more frequent in diabetics as compared to nondiabetics. Other etiological forms of heart diseases include hypertensive heart disease and diabetic cardiomyopathy. Rarely, hemochromatosis may involve pancreas and the heart muscle to produce diabetes mellitus as well as congestive heart failure.

So far, it has been possible to correlate the metabolic abnormalities in diabetes mellitus with cardiac involvement. In a well controlled DM patients, the energy requirements are met by oxidative phosphorylation of fatty acids with glycolytic pathways serving as backup systems. Breakdown of carbohydrates can proceed anaerobically for a short while but complete generation of adenosine triphosphate (ATP) requires oxidative phosphorylation. Proteins do not serve as a major source of ATP except during starvation. Energy utilization in uncontrolled diabetes is characterized by non-utilization of carbohydrates. Fatty acids and ketones serve as the major source of ATP when diabetes is poorly controlled.

Cardiac involvement in diabetes mellitus is characterized by vascular as well as interstitial changes. Vascular involvement is divided into macrovascular (epicardial vessels) and microvascular (small and medium sized intramural vessels) types. Macrovascular involvement, the commonest variety, consists of atherosclerosis. Hyperglycemia directly influences the atherosclerosis development, progression and instability. The principle vascular pertubations linked to hyperglycemia include endothelial dysfunction, vascular effects of advanced glycation end products, adverse effects of circulating free fatty acids and increased systemic inflammation. Endothelial dysfunction, the hallmark of diabetic vascular disease is associated with adverse CVD outcomes. The mechanism contributing to endothelial dysfunction includes abnormal nitric acid biology, increased endothelin, angiotensin 2, and reduced prostacyclin activity, all of which contribute to abnormal control of blood flow. Abnormal lipid metabolism also contributes to increased atherosclerotic risk associated with diabetes. Pertubations in the proteo-fibrinolytic system further compound the direct vascular effects of diabetes. This include increased circulating tissue factor, factor 7, von Willebrand factor, plasminogen activator inhibitor 1 and decreased levels of antithrombin 3 and protein C. Microvascular involvement occurs only rarely without macrovascular involvement. It consists of endothelial damage, basement membrane thickening and microthrombi formation due to increased platelet aggregation. Microaneurysms and proliferative lesions involving small myocardial vessels have also been detected in diabetic patients. Their significance is not yet clear.

Interstitial involvement in diabetes consists of deposition of PAS positive glycoprotein and extensive fibrosis. Though these changes are not unique to diabetes mellitus, the severity of changes in diabetes mellitus is notable especially in those dying of congestive heart failure. The interstitial changes may also be responsible for diastolic dysfunction of the heart in diabetes mellitus.


Coronary artery disease is one of the most significant causes of death in diabetes mellitus. As compared to the general population, there is greater prevalence of coronary artery disease in diabetics. In autopsy studies, the relative risk has been estimated to be 2½ times. Mortality rates from atherosclerotic heart disease in patients attending diabetic clinics have been twice as those of the general population.

Population studies have also revealed that diabetics are twice as likely to develop atherosclerotic heart disease. Framingham study also revealed that the risk of atherosclerotic coronary artery disease in diabetic women is 3 times more common than nondiabetic women and men.

Not only is the risk of atherosclerotic coronary artery disease increased in diabetics, the severity of atherosclerosis is also accentuated by diabetes mellitus. Diabetics generally have coronary heart disease and a higher incidence of multivessel disease. The severity of coronary artery involvement is not related to the duration of diabetes mellitus.

Coronary artery involvement is a feature of T2 DM as well as T1 DM. Therefore clinical manifestations of coronary artery disease are common in young as well as middle aged and elderly patients of diabetes mellitus. The progression of atherosclerotic coronary artery disease is not related to the severity of diabetes mellitus.

Diabetes Mellitus often occurs in the presence of other risk factors for atherosclerosis. Simultaneous occurrence of multiple risk factors is a known phenomenon. The higher prevalence of hypertension in diabetics is well documented. There is also a close relationship between hyperglycemia and hypertriglyceridemia. This relationship is especially strong in T1 DM. Higher incidence of elevated cholesterol levels has also been reported in Diabetic population.

HDL cholesterol levels in women Diabetics have been reported to be low. However, other studies have documented high HDL cholesterol levels in middle aged Diabetics as compared to age and sex matched nondiabetic controls.

Clinical manifestations of coronary heart disease in the diabetic patients are same as in non diabetics i.e. angina, myocardial infarction, heart failure, arrhythmias or sudden death. However, there are some important variations in the clinical profile. Symptomatic coronary artery disease may manifest in young diabetics as early as in their twenties. Symptoms are often atypical. Chest pain may be atypical or absent. Several symptoms represent angina equivalents. Examples include fatigue, dyspnoea, vomiting or unexplained nausea. Chest pain may be altogether absent even during acute myocardial infarction (silent Infarct). Pain was absent in nearly 42 percent diabetics who developed acute myocardial infarction in one study. In Framinghan study 23% of ECG documented myocardial infarction were asymptomatic. Diminished pain sensitivity in diabetes mellitus may be related to diabetic autonomic neuropathy.

In hospital mortality rate from myocardial infarction is higher in diabetics as compared to nondiabetics. The risk of death is approximately twice as high. Excess risk of death from myocardial infarction is present in all ages and in both the sexes, though the risk is highest among young patients and women.

The incidence of heart failure from myocardial infarction is higher in diabetic patients, especially women. Cardiogenic shock, myocardial rupture and recurrence of myocardial infarction are also more common in diabetic patients. Well controlled diabetes mellitus is associated with nearly same prognosis as that in non-diabetics. The prognosis is certainly worse when diabetes is poorly controlled. There is no difference between those taking insulin and patients taking oral anti-diabetic drugs. The incidence of primary ventricular fibrillation may be higher in diabetics, especially those on oral anti-diabetic drugs. Ventricular fibrillation in late hospital phase is also more common in diabetics who develop myocardial infarction.⁽¹âµË’¹â¶â¾ Atrial fibrillation and left bundle branch block were also found to be more common in diabetics in the Swedish cooperative study.

Management of acute myocardial infarction in diabetic patients is similar to that of non-diabetics. Diabetes Mellitus should be controlled with insulin during hospital stay. Blood pressure should be kept in the range of 150-200mg/dl. Insulin induced hypotension, tachycardia, and hypokalemia should be avoided. Hyperglycemia per se can lead to hemodynamic instability and should be prevented.


There is a marked increase in the incidence of heart failure in diabetic patients. Diabetic males are twice as likely to develop heart failure as non-diabetics. The risk is even more marked in diabetic women. The occurrence of congestive heart failure in diabetes may not be related to coronary artery disease, hypertension or any other etiological forms of heart disease.⁽²Ë’⁸˒¹âµâ¾ More commonly, one of these factors is present. Some cases of heart failure may be due to diabetic cardiomyopathy. Diastolic dysfunction of myocardium may also be present in some diabetics.


Sinus node dysfunction and atrioventricular conduction disorders have been reported to be more frequent in diabetics.⁽¹âµâ¾These observations need to be confirmed. In Framingham study, the risk of sudden cardiac death was found to be increased in diabetics.


Diabetic patients with myocardial dysfunction or frank congestive heart failure without significant coronary artery disease, hypertension, chronic renal failure or other etiological forms of heart disease are labeled as suffering from diabetic cardiomyopathy. The important mechanisms of diabetic cardiomyopathy are metabolic disturbances (increased free fatty acids, carnitine deficiency, changes in calcium homeostasis), myocardial fibrosis (increase in angiotensin 2, IGF-1, and inflammatory cytokines), small vessel disease (microangiopathy, impaired coronary flow reserve, endothelial dysfunction), cardiac autonomic neuropathy (denervation and alterations in myocardial catecholamine levels) and insulin resistance.⁽¹â¸â¾ Haemodynamic studies of these patients have shown that the left ventricular end diastolic pressure is raised and ejection fraction is depressed. Left ventricle is dilated. Occasionally, predominant diastolic dysfunction is observed with small heart and raised left ventricular end diastolic pressure. Cardiomyopathy often coexists with microangiopathy, but the significance of this finding is controversial and open to debate. At present there is no effective treatment for diabetic cardiomyopathy. Strict glycemic control may prevent the onset and progression of myocardial dysfunction in diabetes mellitus.

Individuals with insulin resistance and T2 DM have elevated levels of plasminogen activator inhibitors (especially PAI-1) and fibrinogen, which enhances the coagulation process and impairs fibrinolysis, thus favoring the development of thrombosis.

In the DCCT, the number of cardiovascular events did not differ between the standard and intensively treated groups. Improvement in the lipid profile of individuals (lower total and low density lipoprotein (LDL) cholesterol, lower triglycerides) suggested that intensive therapy may reduce the risk of cardiovascular morbidity and mortality associated with DM. In the UKPDS, improved glycemic control did not conclusively reduce cardiovascular mortality. Individuals with DM have an increased incidence of congestive heart failure- diabetic cardiomyopathy.