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Case Examples
Detailed Case Examples how Boston Heart Lab’s Diagnostic Service changed Therapy
Case 1
Maria, 48, manager at Insurance giant: Aggressive lipid therapy to reduce risk
Maria, 48, is travelling business woman putting in long days at her east coast offices. She has borderline LDL-C (128mg/dL) and near optimal HDL-C (47 mg/dL) when looking at a standard lipid panel. Her primary care doctor does not recommend any therapy as “you are doing fine”. However, her husband’s doctor who she met at the company’s annual fall retreat recommended her taking the Boston Heart Lab Test as ”you want to prevent what may be lurking around the corner”. She takes the test and the test reveals the following: high Lp(a), 58mg/dL, which niacin therapy could lower. She also has the FactorV Leiden mutation which puts her at increased risk for deep vein thrombosis. This indicates aspirin therapy when travelling. Her HDL Fingerprint also reveals she has high preβ-1 and low alpha-, a particle profile associated with increased risk of heart disease – again suggesting therapy – statin and maybe niacin. Her primary care doctor gets the results and together they discuss her options and decide to start therapy with Simvastatin and Niaspan. The hot flushes, a side effect from Niaspan, are reduced significantly as she also take aspirin prior to each dose. Overall she feels great to know she does whatever is possible to stay healthy so she can continue working hard which she loves
Case 2
Hunter, 48, high school teacher: Hyperabsorber, non- responsive to high dose statin
Hunter, 49 year old male with previous MI: LDL-C 100 mg/dL, low HDL-C (35 mg/dL), had just switched from 10 Crestor to 20 Crestor without additional LDL-C lowering. TG 145 (just below normal). BHL test reveals he is a cholesterol absorber and thus a candidate for ezetimibe: despite Crestor he has low alpha-1 and -2 and elevated preβ-1. His LpPLA2 is also elevated. In addition, he has low adiponectin level –likely due to slight overweight. It was decided he needs dietary advice (he will see a dietician twice a week for 6 weeks) and is to implement an exercise plan. He is switched to Vytorin 40/10 (Simvastatin and Ezetimibe) and Niaspan (goal 1500mg/day). Two months later Hunter comes back and has lost 4 pounds, and his adiponectin had gone up and was now normal. His LDL-C dropped to 72 mg/dl, TG to 119, and his HDL Fingerprint was almost normal. HDL-cholesterol was now 43.
Case 3
Robert, 59, GM autoworker: Changes to “live a little” as a retiree
Man, 59, slightly overweight, about to retire from one of GM’ s autoplants in Detroit. Has been on Simvastatin (Zocor) 40 for years, LDL is 110, TG 139, HDL 39. His brother age 63 just had a fatal MI. Concerned about his own health he wants to take action. He wants to be able to retire and live a little. The standard lipid panel says he is doing fine, he could possibly increase the Simvastatin to 40 mg. However, his doc wants to do everything he can for Robert so he orders the Complete One from Boston Heart Lab. The test shows his HDL Fingerprint has low alpha-1 and alpha-2, elevated alpha-4 and preB1. He suggest Rob switch to 20 Crestor to increase HDL and drive down LDL. The sterol test also suggests he is a hyperabsorber – so add ezetimibe. These actions may also reduce his elevated hsCRP (2.9) and lower LpPLA2 which was 299 (much elevated). His insulin was borderline high, as was adiponectin, HbA1c and glycosylated albumin. Robert should initiate a regular exercise regimen and dietary changes to lose weight and also reduce the risk of becoming a diabetic. He gets to work with dietician. Rob will return in 8 weeks for a new HDL Fingerprint and diabetes marker checkup.
Case 4
John, 56, mechanic: Aggressive statin and niacin therapy normalizes lipid profile
John, a 54 year old male working as a mechanic at a local service station. He developed chest pain on exertion, went to see his doctor and had a positive stress test. He underwent cardiac catheterization revealing a 85 % blockage in his left anterior descending coronary artery as well as a 90% blockage in his right coronary artery. He underwent angioplasty at the time of his catheterization and had two drug eluting stents placed. He was placed on atorvastatin (Lipitor) 40 mg/day to lower his cholesterol level which was over 240 mg/dl, clopidogrel (Plavix) 75 mg/day to keep his stents open, atenolol (Tenormin) 50 mg/day to control his blood pressure, and enalopril 10 mg/day to also control his blood pressure.
On this regimen his total cholesterol and low density lipoprotein (LDL) cholesterol are “under good control” (i.e. less than 200 mg/dl and less than 100 mg/dl, respectively), and his blood pressure is well controlled by history. He has no history of diabetes, but has a positive family history (father died of a heart attack at age 62). The patient has no history of smoking or diabetes. He does well under age 56 years, when he again develops significant chest pain at rest, and seen in the emergency room, and told that he is having an inferior wall myocardial infarction (heart attack). He is admitted to the hospital, and undergoes cardiac catheterization revealing additional coronary artery disease narrowing in his right coronary artery of 95% past the right coronary artery stent, as well as a complete blockage of his left circumflex coronary artery and an 80% narrowing of his left main coronary artery.
He undergoes coronary artery bypass grafting, with an internal mammary graft to his left anterior coronary artery and a saphenous vein graft to his right coronary artery past the blockage. He continues on the above medication. His doctor reports a height of 5’8, a weight of 215 lbs, a blood pressure of 130/80 mmHg, a fasting glucose of 105 mg/dl, a total cholesterol of 174 mg/dl, triglycerides o f 223 mg/dl, and HDL cholesterol of 31 mg/dl, and a calculated LDL cholesterol of 98 mg/dl.
His cardiologist sends a sample to Boston Heart Laboratory which reveals that his numbers are similar at Boston Heart Laboratory, except that his direct LDL cholesterol is 110 mg/dl, and his small dense LDL cholesterol is 48 mg/dl (elevated > 40 mg/dl). Moreover his large alpha-1 HDL particles is decreased at 8 mg/dl, and his lipoprotein (a) is elevated to two fold at 70 mg/dl. His apoE genotype revealed apoE4/3 (more responsive to diet, less responsive to statin). His Factor V Leiden was negative. All other tests performed including sterols were normal, except that the lathosterol value was slightly elevated indicating over production of cholesterol.
The recommendation was made that he participate in a diet and exercise program, and that he be placed on Rosuvastatin (Crestor) 40 mg/day instead of Lipitor (better inhibitor of cholesterol production and better HDL raising statin), and that Niaspan 2 grams per day be added to his regimen to lower his Lp(a) and increase his HDL cholesterol and large HDL particles. Niaspan is the best HDL raising agent and the only agent that lowers Lp(a) (a genetically determined particle that increases risk).
After 4 months another sample is sent to Boston Heart Laboratory on this patient. Now he has lost 18 pounds and feels much better. According to his doctor his blood pressure is now 120/80 mmHg, his fasting glucose is 88 mg/dl, and his total cholesterol is 134 mg/dl, his triglycerides are 132 mg/dl, his HDL cholesterol is 45 mg/dl, and his calculated LDL cholesterol is 63 mg/dl. A sample is sent to Boston Heart Laboratory which reveals a total cholesterol of 135 mg/dl, triglycerides of 137 mg/dl, an HDL cholesterol of 44 mg/dl, and a direct LDL cholesterol of 59 mg/dl (optimal), a small dense LDL cholesterol of 19 mg/dl (optimal), an Lp(a) of 42 mg/dl (still increased, much closer to normal). In addition his plasma sterols were now normal and his his large alpha-1 HDL apoA-I level had dramatically increased to 21 mg/dl (well into the normal range where regression of coronary atherosclerosis can be achieved.
In this case having his sample sent to Boston Heart Laboratory allowed for the detection of elevated Lp(a), and an optimization of his statin therapy and the addition of niacin therapy which lowered his Lp(a), triglycerides, and small dense LDL cholesterol, and increased his HDL cholesterol and his large HDL particles, markedly reducing his CHD risk.
Case 5
Lou-Ann, 74, retired Walmart cashier: statin intolerant hyperabsorber
A 74 year old woman, a retired Walmart cashier, has a history of angina which is controlled with medication (atenolol 50 mg/day). Her stress tests have been equivocal and her doctor wants to be conservative. She has a history of high blood pressure for which takes enalapril 10 mg/day and hydrochlorthiazide 25 mg/day. She has a history of fatigue and has not been able to take atorvastatin (Lipitor) or simvastatin because of muscle aches and pain, and also her cholesterol levels did not decrease very much. She follows an excellent diet, and walks at least 30 minutes per day with her dog. Her doctor reports a height of 5’2 a weight of 115 lbs, a blood pressure of 130/80 mmHg, a fasting glucose of 84 mg/dl, a total cholesterol of 281 mg/dl, triglycerides o f 120 mg/dl, an HDL cholesterol of 56 mg/dl, and a calculated LDL cholesterol of 201 mg/dl (markedly elevated). Because of her difficulties with statins and lack of response he sends a sample of her blood drawn after an overnight fast to Boston Heart Laboratory.
Her tests revealed a normal apoE and factor V Leiden genotype. Her HDL particles were normal, but she was found to have a direct LDL cholesterol of 198 mg/dl and a small dense LDL cholesterol of 55 mg/dl (both elevated). She was found to have an elevated thyroid stimulating hormone value of 12 uIU/ml, indicating she noted thyroid hormone replacement. Her sterol select testing revealed a marked elevation of beta sitosterol and campesterol consistent with over absorption of cholesterol in the intestine. The recommendation was made that she be placed on thryroid hormone replacement and ezetimibe at a dose of 10 mg/day.
After three months of this therapy her fatigue and cold intolerance disappeared, her thyroid tests were normal, and her total cholesterol was 174 mg/dl, her HDL cholesterol was 61 mg/dl, her triglycerides were 115 mg/dl, and her calculated LDL cholesterol was 90 mg/dl. Knowing she was a hyperabsorber and also hypothyroid made a great difference in her therapy.
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