Understanding Hypertensive Vascular Disease & Atherosclerosis: Overview and Prognosis

1. Diseases of Cardiovascular system Dreamstime.com MaramAbdaljaleel, MD Dermatopathologist and Neuropathologist

2. OBJECTIVES: • HYPERTENSIVE VASCULAR DISEASE • ATHEROSCLEROSIS

3. HYPERTENSIVE VASCULAR DISEASE Dreamstime.com

4. WHY? • 25% of the population • major risk factor for atherosclerosis, congestive heart failure, and renal failure

5. WHAT? • According to the National Heart, Lung, and Blood Institute hypertension is defined as consistent systolic readings of 140 mm Hg or higher or diastolic readings of 90 mm Hg or higher. • Based on research, consistent systolic readings of 130 to 139 mm Hg or diastolic readings of 80 to 89 mm Hg in patient older than 13 years and have other cardiovascular risk factors (e.g., diabetes) is considered Hypertension

6. Prognosis: • Prognosis (without appropriate treatment): • 50% die of ischemic heart disease (IHD) or congestive heart failure • 30% develop stroke.

7. malignant hypertension (accelerated hypertension) • It’s a clinical syndrome characterized by sever hypertension(systolic pressures over 200 mm Hg or diastolic pressures over 120 mmHg), renal failure and retinal hemorrhages and exudate with or without papilledema. • Prognosis: presenting with a rapidly rising blood pressure if untreated leads to death in within 1 to 2 years.

8. idiopathic (essential hypertension): • 90-95% • compatible with long life unless a myocardial infarction, stroke, or another complication supervenes. • Complex, multifactorial disorder resulting from interaction of mutations, polymorphisms, with variety of environmental factors. • Single gene disorders cause sever but rare forms of hypertension

9. Cont. Single gene disorders: • Gene defects in enzymes involved in aldosterone metabolism (e.g., aldosterone synthase, 11β-hydroxylase, 17α-hydroxylase), leading to increased aldosterone secretion, increased salt and water resorption, and plasma volume expansion • Mutations in proteins that affect sodium resorption(as in Liddle syndrome, which leads to increased distal tubular resorption of sodium induced by aldosterone)

10. secondary hypertension • 5% • Caused by: • Renal: Acute GN, Chronic renal disease , Polycystic disease, Renal artery stenosis, Renal vasculitis, Renin-producing tumors • Endocrine: Adrenocortical hyperfunction (Cushing syndrome, primary aldosteronism, congenital adrenal hyperplasia), Exogenous hormones (glucocorticoids, estrogen, and sympathomimetics), Pheochromocytoma, Acromegaly, Hypothyroidism, Hyperthyroidism , Pregnancy-induced (pre-eclampsia). • Cardiovascular:Coarctationof aorta, PAN, Increased intravascular volume, Increased CO, rigidity of the aorta. • Neurologic: Psychogenic, Increased intracranial pressure, Sleep apnea, acute stress (surgery)

11. morphology • accelerates atherogenesis • degenerative changes in the walls of large and medium sizedarteries that can lead to aortic dissection and cerebrovascular hemorrhage. • small blood vessel disease: • hyaline arteriolosclerosis • hyperplastic arteriolosclerosis

12. hyaline arteriolosclerosis • associated with benign hypertensionbut can be seen also in elderly patients and diabetic microangiopathy • Histology: homogeneous, pink hyaline thickening of the arteriolar walls, with luminal narrowing.

14. hyperplastic arteriolosclerosis • typical of severe hypertension. • Histology: “onionskin” concentric, laminated thickening of arteriolar walls and luminal narrowing. The laminations consist of smooth muscle cells and thickened, reduplicated basement membrane. • accompanied by fibrinoid deposits and vessel wall necrosis (necrotizing arteriolitis), especially in the kidney.

16. www.123rf.com

17. WHAT? • Characterized by intimal lesions called atheromas (atherosclerotic plaques) that protrude into vascular lumina. • Atherosclerotic plaque consists of raised lesion with soft yellow core of cholesterol, cholesterol esters and necrotic debris covered by fibrous cap.

19. WHY? • Prevalent in most developed nations • The mortality rate for IHD in the United States is among the highest in the world (including people who adopts American life styles and dietary customs acquire the same atherosclerosisrisk as for U.S. born persons)

20. Risk factors WHEN? “ These risk factors have roughly multiplicative effects.” • Major constitutional risk factors • Major modifiable risk factors

21. Major constitutional risk factors • Genetics - Family history is the most important independent risk factor. Most familial risks are related to hypertension or diabetes • Or less commonly Familial hyperlipidemia , specifically hypercholesteremia

22. b. Age : • Between ages 40 and 60, the incidence of myocardial infarction in men increases fivefold. • Death rates from IHD continue to rise with each successive decade. c. Gender - Premenopausal women are relatively protected against atherosclerosis. - After menopause, the incidence of atherosclerosis-related diseases increases and with greater age eventually exceeds that of men.

23. II. Major modifiable risk factors 1. Hyperlipidemia • The low-density lipoprotein (LDL) cholesterol ("bad cholesterol"); has an essential physiologic role delivering cholesterol to peripheral tissues. • In contrast, high-density lipoprotein (HDL, "good cholesterol") mobilizes cholesterol from atheromas and transports it to the liver for excretion in the bile. • Consequently, higher levels of HDL correlate with reduced risk. • High dietary intake of cholesterol and saturated fats (present in egg yolks, animal fats, and butter, for example) raises plasma cholesterol levels. • diets low in cholesterol and/or with higher ratios of polyunsaturated fats lower plasma cholesterol levels.

24. 2. Hypertension: • increase the risk of IHD by approximately 60%. 3. Cigarette Smoking: • Prolonged smoking of one pack daily increases the death from IHD by 200%. Smoking cessation reduces that risk substantially. 4- Diabetes Mellitus: • The incidence of myocardial infarction is twice as in non-diabetic individuals. • There is also an increased risk of strokes and a 100-fold increase • Increased risk of atherosclerosis-induced gangrene of lower extremities.

25. MORPHOLOGY • Fatty Streaks: • begin as minute yellow, flat macules composed of lipid-filled foamy macrophages • only minimally raised and do not cause significant flow disturbance. • Present in aortas of infants <1 year and in virtually all children >10 years, regardless of genetic, clinical, or dietary risk factors. • Atherosclerotic Plaque: • white to yellow raised lesions; they range from 0.3 to 1.5 cm in diameter but can coalesce to form larger masses. • patchy, involving only a portion of arterial wall “eccentric”

26. Aorta with fatty streaks mainly near the ostia of branch vessels. Fatty streak demonstrating intimal, macrophage-derived foam cells

27. Distribution: • In descending order, the most extensively involved vessels are the infrarenal abdominal aorta, coronary arteries, popliteal arteries, Internal carotid arteries, and vessels of the circle of Willis. • more severe in the abdominal aorta than in the thoracic aorta. • Vessels of the upper extremities usually are spared • mesenteric and renal arteries are spared except at their ostia.

28. Symptomatic atherosclerotic disease Most often involves: a. Coronary arteries causing , Myocardial infarction (heart attack), b. Cerebral vessels causing cerebral infarction (stroke), c. Lower extremities: peripheral vascular disease (gangrene of the legs) d. Aortic aneurysms

29. Clinical complications of atherosclerotic plaques: • Rupture, ulceration, or erosion of the luminal surface of atheromatousplaques induces thrombus formation leading to tissue ischemia (heart). If the patient survives, thrombi become organized and incorporated into the growing plaque. • Hemorrhage into a plaque resulting in hematoma formation and may cause rapid plaque expansion or plaque rupture.

30. Cont. • Atheroembolism. Ruptured plaque can discharge debris into the blood, producing microemboli • Aneurysm formation. Due to pressure or ischemic atrophy of the underlying media, with loss of elastic tissue, causes structural weakening that can lead to aneurysmal dilation and rupture.

31. primary prevention programs Primary programs include; a. Cessation of cigarette smoking b. Control of hypertension, c. Weight loss, exercise, d. Lowering LDL blood cholesterol levels while increasing HDL ( by diet or statins).

32. Secondary prevention programs • to prevent recurrence of events such as myocardial infarction or stroke in symptomatic patients and involves: a. The use of aspirin (anti-platelet agent), b. Statins, c. Beta blockers (to limit cardiac demand), d. as well as surgical interventions (e.g., coronary artery bypass surgery, carotid endarterectomy). - These can successfully reduce recurrent myocardial or cerebral events

33. THANK YOU