1. Create a Client Centered Pathophysiology. Case Retro Analysis (Case A)A 49-year-old woman was referred to department for a cardiological follow-up visit. She had amedical history of hypertension and previous MI, with no history of diabetes mellitus,hypercholesterolemia or premature coronary artery disease in her family. She did not smoke, takerecreational drugs and was not on oestrogen replacement therapy.Ten years earlier, she had an inferior MI treated with systemic thrombolysis, unfractioned heparin,aspirin, atenolol and intravenous nitroglycerine. During her hospitalization, the echocardiogram(ECG) revealed akinesis of the posterior-basal wall with an estimated ejection fraction of 50%.Laboratory tests including serum glucose, lipids, blood count, liver-, kidney- and thyroid-functiontests were within normal limits. The day before her discharge, she had a stress ECG negative forinducible ischemia. The patient was discharged on the sixth day with a drug regimen of aspirin,atenolol, captopril, simvastatin and isosorbide dinitrate.After the MI and prior to the visit to our department, the patient had been free from chest pain anddyspnea and had a normal exercise tolerance. She had periodical ECGS that showed thepresence of akinesis of the posterior-basal wall with a mildly depressed systolic function. Shereported a good control of arterial blood pressure with the ongoing therapy, including perindopril5 mg/day, hydroclhorotyazide 25 mg/day and atenolol 25 mg/day associated with aspirin andsimvastatin 20 mg/day.A physical examination showed blood pressure of 135/80 mmHg, heart rate of 64 bpm, BMI of 27kg/m2, waist circumference of 85 cm and no findings of congestive heart failure. The resting ECGshowed a sinus rhythm at 62 bpm and the presence of Q waves in II, III and aVF leads with noother abnormalities.Laboratory tests revealed a total serum cholesterol of 160 mg/dl, HDL cholesterol of 55 mg/dl,triglycerides of 78 mg/dl, LDL cholesterol of 89.6 mg/dl and fasting glycemia of 116 mg/dl, with anormal OGTT and normal plasma homocysteine.On the basis of her medical records concerning the MI, she was confirmed the diagnosis ofcoronary artery disease (CAD) according to the recently published universal definition of MI.For risk stratification, she was studied with non-invasive diagnostic tests, includingechocardiography and a treadmill exercise test.The ECG confirmed the presence of akinesis of the posterior-basal wall with a mildly depressedsystolic function (LVEF 48%) and the treadmill exercise test showed no signs of inducibleischemia.The MSCT angiographic analysis showed no coronary lesions but the presence of a hypodensearea involving more than 50% of the myocardial wall of the left ventricular inferior basal portion.No lesions were detected in the wholly explored extra-coronary arterial system.The patient was sent to follow-up with a drug regimen of perindopril 5 mg/day andhydrochlorothiazide 25 mg/day. Aspirin, atenolol and simvastatin were discontinued. She wasadvised to lose weight and implement some lifestyle changes and was asked to repeat laboratorytests for a lipid profile before the next follow-up visit.At the 6- and 12-month follow-up, the patient was free from chest pain, LDL-cholesterol was below140 mg/dl without statin therapy and blood pressure was stable below 140/90 mmHg.

Question

1.	Create a Client Centered Pathophysiology. Case Retro Analysis (Case A)A 49-year-old woman was referred to department for a cardiological follow-up visit. She had amedical history of hypertension and previous MI, with no history of diabetes mellitus,hypercholesterolemia or premature coronary artery disease in her family. She did not smoke, takerecreational drugs and was not on oestrogen replacement therapy.Ten years earlier, she had an inferior MI treated with systemic thrombolysis, unfractioned heparin,aspirin, atenolol and intravenous nitroglycerine. During her hospitalization, the echocardiogram(ECG) revealed akinesis of the posterior-basal wall with an estimated ejection fraction of 50%.Laboratory tests including serum glucose, lipids, blood count, liver-, kidney- and thyroid-functiontests were within normal limits. The day before her discharge, she had a stress ECG negative forinducible ischemia. The patient was discharged on the sixth day with a drug regimen of aspirin,atenolol, captopril, simvastatin and isosorbide dinitrate.After the MI and prior to the visit to our department, the patient had been free from chest pain anddyspnea and had a normal exercise tolerance. She had periodical ECGS that showed thepresence of akinesis of the posterior-basal wall with a mildly depressed systolic function. Shereported a good control of arterial blood pressure with the ongoing therapy, including perindopril5 mg/day, hydroclhorotyazide 25 mg/day and atenolol 25 mg/day associated with aspirin andsimvastatin 20 mg/day.A physical examination showed blood pressure of 135/80 mmHg, heart rate of 64 bpm, BMI of 27kg/m2, waist circumference of 85 cm and no findings of congestive heart failure. The resting ECGshowed a sinus rhythm at 62 bpm and the presence of Q waves in II, III and aVF leads with noother abnormalities.Laboratory tests revealed a total serum cholesterol of 160 mg/dl, HDL cholesterol of 55 mg/dl,triglycerides of 78 mg/dl, LDL cholesterol of 89.6 mg/dl and fasting glycemia of 116 mg/dl, with anormal OGTT and normal plasma homocysteine.On the basis of her medical records concerning the MI, she was confirmed the diagnosis ofcoronary artery disease (CAD) according to the recently published universal definition of MI.For risk stratification, she was studied with non-invasive diagnostic tests, includingechocardiography and a treadmill exercise test.The ECG confirmed the presence of akinesis of the posterior-basal wall with a mildly depressedsystolic function (LVEF 48%) and the treadmill exercise test showed no signs of inducibleischemia.The MSCT angiographic analysis showed no coronary lesions but the presence of a hypodensearea involving more than 50% of the myocardial wall of the left ventricular inferior basal portion.No lesions were detected in the wholly explored extra-coronary arterial system.The patient was sent to follow-up with a drug regimen of perindopril 5 mg/day andhydrochlorothiazide 25 mg/day. Aspirin, atenolol and simvastatin were discontinued. She wasadvised to lose weight and implement some lifestyle changes and was asked to repeat laboratorytests for a lipid profile before the next follow-up visit.At the 6- and 12-month follow-up, the patient was free from chest pain, LDL-cholesterol was below140 mg/dl without statin therapy and blood pressure was stable below 140/90 mmHg.

Accepted Answer

When coronary blood flow is reduced, a myocardial infarction occurs.
Atherosclerotic plaque rupture…