“Mr. A.D,” a 28 year-old Hispanic married man reported at the endocrine clinic for his follow up of labs, without prior appointment. Mr. A.D. reported at the clinic after a telephonic reminder, because he failed to turn up as per schedule of his labs and follow up treatment for hyperlipidemia. The reason for his failed appointment was cited as his preoccupation in attending a social function. He complained of giddiness while driving and asphyxiated at his work place, an automobile service station.
Mr. A.D reported that he was diagnosed for diabetes and dyslipidemia. It derived that Mr. A.D was obese, and had high cholesterol related complications during his teenage years. On subjective analysis it was noticed that understanding patient’s past medical history is significant in clinical observation as it revealed that he had past medical history of Pancreatits and Hyperlipidemia, and had surgery for spleen removal, Pancreatectomy, and Gall bladder removal. It was reported that his family also had history of diabetes, hypertension, and hyperlipidemia. His father is diabetic, with hypertension, and his mother and brother had hyperlipidemia. Mr. A.D is a nonsmoker and nonalcoholic and is married with two healthy boys.
Examination of vital signs showed that Mr. A. D was alert and oriented; though his eyes were jaundiced, and lips were dry. His lung was clear to ausculate and heart beat was in regular rhythm, and investigation of stomach revealed no visible mass, nor tenderness with visible pulsation.
Subjectively Mr. A.D was feeling well, and had presence of bowel movement, and he was voiding well with no difficulties. His body temperature at the time of reporting was recorded as 97.8, blood pressure at 112/68, and pulse rate of 80. Baseline information, such as age, body frame size, current medical condition, medication use, and previous hospitalization as well as blood pressure and blood lipid levels were ascertained and recorded Blood samples for cholesterol measurement were collected with specific instruction to diagnose total cholesterol level, lipoprotein level, and triglyceride level
His endocrinologist already put him on no fat diet, and the active prescription of medication included novolog (sliding scale), Lantus 25 units before hours of sleep, magnesium oxide 1 tab three times/day for 10 days, Ursodol 300 mg three times/day, and Lovaza 4mg/day
Black and Hispanic Americans generally have lower insurance coverage rates and poorer access to care. Cardiovascular risk factors identified for Hispanics are obesity, hypertension, dyslipidemia, and type 2 diabetes mellitus, which is compounded with lack of physical activity, smoking, and excessive drinking, “and heart disease is the leading cause of death among Hispanics.” (Ferdinand).
Investigations have revealed that incidence of coronary artery disease (CAD) and total and low-density lipoprotein (LDL) cholesterol levels are intrinsically interwoven. It is estimated that “approximately 1.5 million Americans experience an acute myocardial infarction, and one-third of them do not survive” (Ellis & Sprecher, 2002). “Dyslipidemias are disorders of lipoproteins metabolism, including lipoprotein overproduction or deficiency, which may be manifested by elevation of serum total cholesterol, low-density lipoprotein (LDL) cholesterol and triglyceride concentration, and a decrease in the high-density lipoprotein (HDL) cholesterol concentration.” (Ahmed et al, 1998).
Secondary causes of dyslipidemia include hyperthyroidism, and a genetic predisposition, which are classified as “familial hypercholesterolemia, familial combined hyperlipidemia and polygenic hypercholesterolemia” (Ahmed, et al, 1998). “Hyperlipidemia is an excess of fatty substances called lipids, largely cholesterol and triglycerides, in the blood” and these fatty substances travel in the blood attached to proteins. (Health encyclopedia-diseases and conditions, 2009). Two subcategories of hyperlipidemia are hypercholesterolemia and hypertriglyceridemia, in which there is high level of either cholesterol or triglycerides.
The cholesterol circulating in the blood can be classified into good and bad cholesterol, and two classes are high density lipoprotein (HDL) and low density lipoprotein (LDL) cholesterol. HDL cholesterol helps reduce the deposits and decrease the atherosclerotic changes, whereas LDL cholesterol deposits in the arteries leading to hardening of the arteries. Common causes of hypercholesterolemia include low thyroid hormone levels, pregnancy and kidney failure, and hypertriglyceridemia include diabetes, excess alcohol intake, obesity, and certain prescription medications.
Ceriello (2008) points out that ‘in the presence of hyperglycaemia, proteins and lipids are irreversibly glycated by non-enzymatic mechanisms, and these advanced glycated end products (AGEs) accumulate in the cells and extracellular space of blood vessels, enhancing atherogenic processes.’ When a fatty streak develops on an arterial wall, which is formed by clustering of monocytes in response to lipoprotein oxidation or other influence, onset of atherosclerosis is predictable. In addition, production of collagen, leading to the formation of hard fibrous plaques, also contributes to atherosclerotic plaque. Consequent to increase in volume of arterial plaque coronary artery expands outward to facilitate blood flow through stenosed vessel segment, and continues till it reaches maximum point of flexibility. Further accumulation of fibrous tissues leads to formation of fibrous cap, and the ‘progressive arterial stenosis eventually lead to ischemic vascular disease,’ and the rupture of a plaque causes myocardial infarction.
The primary clinical manifestations of dyslipidemia are “ischemic vascular disease, pancreatitis, and xanthomatosis” (Ellis & Sprecher, 2002). Since hyperlipidemia usually has no noticeable symptoms, except deposits of cholesterol under the skin (called xanthomatosis), especially around the eyes or along the Achilles tendon, it may be detected only during routine examination or evaluation for atherosclerotic cardiovascular disease. Many pimple-like lesions across body of an individual may indicate presence of hypertriglyceridemia, and high levels of triglycerides may result in sever inflammation of the pancreas. Testing for hyperlipidemia is done by blood test after overnight fasting, and then analyzing to determine types and levels of cholesterol and lipids. Maintaining the optimal HDL cholesterol and triglyceride levels between >40 mg/dl and <200 mg/dl is the agreed upon target. (Chen, H, 2005; Health encyclopedia-diseases and conditions, 2009).
Studies indicate that ‘control of acute hyperglycaemia improves survival among patients with acute coronary syndrome and MI’, as hyperglycaemia has been independently associated with “left ventricular dysfunction, larger infarct size, increased thrombophilia and acute increases in inflammatory immune markers” among patients with MI. (Ceriello, A., 2008). Another study analyzing the association of postprandial hyperglycaemia (PPH) and myocardial perfusion defects suggest that there was a significant correlation between changes in blood volume and the degree of PPH in diabetic patients and myocardial perfusion defects are related to impaired coronary microvascular circulation. A prospective diabetes study group in the United Kingdom found that “intensive control of fasting blood glucose (FBG) among diabetes patients reduced the relative risk for myocardial infarction (MI) by only 16% as compared to conventional, diet-based therapy.” (Ceriello, A., 2008).
Literature reviews reveal that the difficulty in treating lipid disturbance has been the “coexistence of elevated triglycerides with other conditions that affect cardiovascular disease risk, such as depressed high-density lipoprotein-cholesterol, obesity, metabolic syndrome, proinflmmatory and prothrombotic biomarkers, and type 2 diabetes.” (Yuan, 2007).
“Angiographic studies show that aggressive cholesterol reduction by a variety of methods, as opposed to dietary modification alone, results in increased rates of plaque regression and stabilization.” (Ahmed et al, 1998). It is recommended that patients with pre-existing coronary disease, peripheral artery disease, carotid stenosis, aortic aneurysm, diabetes or an over 10-year risk of greater than 20 percent of having a cardiac event should maintain their LDL cholesterol levels below 100 mg per dL.
A patient with coronary heart disease, with LDL levels less than 100 mg per dL should begin dietary therapy, and engage in regular physical activity. Dietary therapy aims to decrease the IDL cholesterol level to the target values, while maintaining nutritious diet, and step I and step II diets are designed to progressively reduce intake of saturated fats, cholesterol and total calories. Main emphasis of dietary therapy is on complex carbohydrates, rather than sugars. ”The step I diet has been shown to lower the total serum cholesterol level by 3 to 14 percent, while the step II may lower an additional 3 to 7 percent” of total cholesterol level (Ahmed, et al, 1998). A less fat diet containing less than 30 per cent of total calories and saturated fat is found to reduce LDL cholesterol levels in some patients, and a high-fiber diet is also therapeutic. Exercise programs that are tailored to meet individual goals, interests, and needs are beneficial and overweight patients should engage in low-intensity exercise more frequently and for longer duration. Patients with multiple risk factors for coronary health disease, even without a history of coronary heart disease, should be treated aggressively, as “primary and secondary prevention are closely linked” (Ahmed, et al, 1998). Exercise is a non-pharmacological, low-cost intervention commonly recommended to optimize lipid and lipoprotein. However, a meta-analysis by Kelly & Kelly (2008) to examine the effects of aerobic exercises on non-high-density lipoprotein cholesterol in children and adolescents found that “aerobics does not reduce non-HDL-C but does improve percent body fat.” Even though studies indicate contradicting results regular exercise under expert guidance is more beneficial in reducing body weight and controlling maladies associated with obesity.
Most common pharmacologic treatment options for dyslipidemia include bile acidbinding resins, HMG –CoA reductase inhibitors, nicotinic acid and fibric acid derivatives. “Lovastatin (Mevacor), pravastatin (Pravachol), simvastatin (Zocor), fluvastatin (Lescol), atorvastatin (Lipitor), and ceivastatin (Bacycol) are HMG-CoA reducatase inhibitors, or statins, that inhibit cholesterol synthesis” (Ahmed, et al, 1998). Four main classes of medications are recommended in the treatment of hyperlipidemia, such as statin medications, niacin, the fibrates, and the cholesterol absorption inhibitors (CAIs), which primarily act in lowering LDL cholesterol.
Statin medications generally contain Lipitor, Zocor, Pravachol, Lesol, and Crestor. Niacin, a common B vitamin, is found to increase HDL when used with a statin. The purpose of fibrates is to lower triglycerides. Cholesterol absorption inhibitors like Zeta decrease cholesterol levels by affecting its absorption from the intestinal system. Though statins are standard medication for hyperlipidemia, combination medication may also be adopted after ensuring that the potential for drug interactions and negative side effects is kept to a minimum.
MR. A.D has to be considered as case of “familial combined hyperlipidemia,” which is genetic, and the “most common disorder of increased blood fats that causes early heart attacks” because he has a family history of first degree relative with dyslipidemia. (Health guide: Familial combined hyperlipidemia, 2009).
The intervention comprised an initial screening of Mr. A.D for comprehensive risk assessment, patient education, and lifestyle counseling. Thereafter, laboratory test values, and other risk factors present were analyzed. The patient was apprised about the condition and discussed the recommended schedule of regular medical tests, provided instruction on dietary changes, educated the benefits of regular exercise, and importance of medication was highlighted. Since dietary modifications are found to be slow and less effective in reducing LDL cholesterol levels it is recommended that cholesterol-lowering agents should be considered if a patient has very high LDL cholesterol level or lipid levels remain elevated after six months of intensive dietary therapy. Mr.A.D was recommended to follow combination medication with statin and to undergo measurement of fasting total cholesterol, LDL cholesterol, high-density lipoprotein (HDL cholesterol, and triglyceride levels every week without fail. Since Mr. A.D has a family history of diabetes, hypertension and dyslipidemia, and he himself had bitter experience from these maladies he has been instructed to screen his children also for obesity and diabetes, though they are reported to be healthy. Introducing life style changes like adopting fat free fiber rich food and engaging in regular exercise for the entire family was also highlighted. Though Mr. A.D. has shown much interest in following instructions it has to be construed that his social, economical, and cultural background is not conducive for bringing changes. It may be worth noting that he did not report for labs on the appointed day because he was more interested to participate in a social function rather than attending his health needs. Moreover, it has to be construed that Mr. A.D. is more accustomed to his physical and medical condition since it is routine with his family.
Ferdinand, Keith C. Prevention and control of CVD RF policy level, health systems and community: Main issues and perspectives-hypertension.
Ahmed, Syed M., Clasen, Mark E., & Donnelly, John F. (1998). Management of Dyslipidemia in Adults. AFP.
Health encyclopedia-diseases and conditions. (2009). USA Today.
Yuan, George et al. (2007). Hypertringlyceridemia: Its etiology, effects and treatment. PubMed Central.
Health guide: Familial combined hyperlipidemia. (2009). The New York Times.
Note: Model case study articles used for episodic analysis are:
Fenton. W. S, & Chavez, M. R. (2008). Medication-induced weight gain and dyslipidemia in patients with schizophrenia. American Psychiatric Association, 6: 246-253.
Babington, K. K, & Dewitt, D. E. (2006). The meaning of autoantibody titers, exercise, and alcohol in a thin 65-year-old man hospitalized for cholangitis and coincidental new diabetes. Case study. Clinical diabetes, 24: 185-186. Web.
Ceriello, A. (2008). Review: Cardiovascular effects of acute hyperglycaemia: pathophysiological underpinnings. Diabetes and vascular disease research, 5(4); 260-269.
Ellis, K., & Sprecher, D. L. (2002). Hyperlipidemia. Medicine index. Cleveland clinic. Web.
Kelly, G. A., & Kelly, K. S. (2008). Effects of aerobic exercise on non-HDL-C in children and adolescents: A meta-analysis of randomized controlled trials. PubMed Central. Web.