Cardioascular Disorders for the lectv.pptx

therapeutic

1. Cardiovascular Disorders 1

2. risk factors for cardiovascular disease The most important behavioral risk factors of heart disease and stroke are unhealthy diet, physical inactivity, tobacco use and harmful use of alcohol. The effects of behavioral risk factors may show up in individuals as raised blood pressure, raised blood glucose, raised blood lipids, and overweight and obesity.   Cardiovascular disease (CVD) : are a group of disorders of the heart and blood vessels. 2

3. Classical and novel cardiovascular risk factors. 3

4. HYPERTENSION Blood pressure classified into four categories:  normal, prehypertension (mild), stage 1 (moderate) and stage 2 (severe) .  An individual is considered to have hypertension based on the average of two or more blood pressure readings following an initial assessment. It can lead to severe health complications and increase the risk of heart disease, stroke, and sometimes death. 4

5. Blood Pressure Classification Mild to moderate hypertension is usually asymptomatic. Secondary hypertension should be considered for severe or resistant hypertension (high BP despite treatment from three medications in different classes including diuretic), an acute rise in previously stable BP, 5

6. secondary hypertension is suggested, a number of conditions need to be considered including primary renal disease, renovascular disease, sleep apnea, coarctation of the aorta (young children), pheochromocytoma , primary aldosteronism . Malignant hypertension: is associated with neurologic symptoms due to intracerebral or subarachnoid bleeding (headache, nausea, vomiting, somnolence, confusion. hypertension risk factors: are family history (2× risk), African descent, obesity, excessive alcohol or salt intake, physical inactivity, dyslipidemia….etc. 6

7. Diagnostic test for hypertension: Most patients with primary hypertension should undergo a limited evaluation due to poor diagnostic yield. Routine lab tests are recommended before beginning treatment of high blood pressure to determine organ or tissue damage or other risk factors. These lab tests include urinalysis, blood cell count, blood chemistry (potassium, sodium, creatinine , fasting glucose, total cholesterol and HDL cholesterol), and an ECG (electrocardiogram). When hypertension is associated with decreased serum potassium, rule out antihypertensive medication. Increased calcium is seen with hyperparathyroidism. 7

8. Hyperlipidemia is an elevation of lipids (cholesterol, cholesterol esters, phospholipids, and triglycerides) in the bloodstream. Diseases That May Cause Dyslipidemia and Associated Lipid Changes 8

9. hyperlipidemia, discovered during routine examination or evaluation for atherosclerotic cardiovascular disease due to There are typically no symptoms associated with hyperlipidemia, Classification of Familial Dyslipidemias 9

10. Laboratory Findings Low-risk persons: Further testing is not required if the HDL-cholesterol level is ≥40 mg/ dL and TC is <200 mg/ dL . High-risk persons: Lipoprotein measurement is recommended as a guide to clinical management. More frequent measurements are required for persons with multiple risk factors. Elevated of apolipoprotein ( LpA ) aid in risk assessment for CHD. Lecithin–cholesterol acyltransferase deficiency is a very rare autosomal recessive disorder of adults.It is associated with premature CAD, 10

11. TG >150 mg/ dL , HDL-C<40 mg/ dL in men and <50 mg/ dL in women, with small dense LDL particles. Abnormalities in fibrinolys is and coagulation. Exclusion of other causes of dyslipidemia ( e.g.,cholestasis , hypothyroidism, chronic renal failure, nephrotic syndrome). Atherogenic Dyslipidemia Familial Hypercholesterolemia (Type II) Familial hypercholesterolemia is inherited as an autosomal dominant disorder. Homozygous patients are very rare (1 per million). Clinical manifestations include increased TC ( xanthomata , corneal arcus , CAD that causes death usually before age 30 years). 11

12. Laboratory Findings TC is very high (600–1,000 mg/ dL ) with corresponding increase in LDL. increased LDL-C and VLDL and chylomicrons; HDL-C is often low. Different members may have increased serum TC or TG or both. Atherosclerosis Atherosclerosis is the condition in which the atheroma (plaque) is found in the arteries as an inflammatory response to injury. The plaques contain lipids, smooth muscle cells, connective tissue, inflammatory cell, and other extracellular constituents. Atherosclerosis is responsible for almost all cases of coronary heart disease. Plaque stability is variable and can rupture, triggering in situ thrombosis or embolization, 27leading to potential acute ischemic events. 12

13. Atherosclerosis Atherosclerosis is the condition in which the atheroma (plaque) is found in the arteries as an inflammatory response to injury. The plaques contain lipids, smooth muscle cells, connective tissue, inflammatory cell, and other extracellular constituents. Atherosclerosis is responsible for almost all cases of coronary heart disease. Plaque stability is variable and can rupture, triggering in situ thrombosis or embolization,leading to potential acute ischemic events. 13

14. occurs over years and is initially asymptomatic until ischemia is clinically manifested. Clinical manifestation is dependent on the particular circulatory bed affected. Manifestations include myocardial infarction and angina, stroke, mesenteric ischemia or renal artery stenosis, aneurysms, and arterial dissection. Risk factors for atherosclerosis include age, gender, cigarette smoking, DM, endothelial dysfunction, dyslipidemia, hypertension, and family history. Atherogenesis 14

15. Laboratory Findings 1- Lp (a) and homocysteine are increased. 2- Elevated CRP (if first result is >3.0 mg/L, repeating the test at least 2 weeks later when patient is in metabolically stable state free of infection or acute illness is recommended). 3- Coronary artery calcium scores exceeding 100 AU ( Agatston units) or 75th percentile are considered high risk for coronary events, as are any carotid plaque or IMT exceeding 75 th percentile. 15

16. Markers of cardiac myocyte necrosis: CK (total) Ck -MB ( isoenzyme of heart) LDH ( Has 5 isoenzymes ) GOT ( transamiase enzyme) Troponin I & T Myoglobin (urine and serum) Homocystain Cardiac Markers “ Cardiac markers are substances released from heart muscle when it is damaged as a result of myocardial infarction.” Note: As will be discussed, it has been shown that cardiac markers can be released from cardiac tissue as a result of damage from processes other than MI 16

17. Occurs when the blood supply to the brain is interrupted Thrombus – blood clot Embolus – free flowing clot Aneurysm – bulging or burst blood vessel Transient ischemic attack (TIA) – brief interruptions that cause temporary impairment Stroke 17

18. Earliest increase 4-8 hours Peak hours 24-36 hours Duration of Increase 36-48 hours Specificity 57-88% Sensitivity at peak 93-100% Laboratory Findings CK Total 18

19. IM injection Traumatic damage to skeletal muscle Hypothermia Exercise Intoxication Dose-related side effect in statin treatment Total CK can be elevated 19

20. Troponin-I levels begin to rise 2-3 hours after onset of MI and roughly 80% of patients with AMI will have positive values at 3 hours Elevations in Troponin-I and Troponin-T can persist for up to 10 days after MI Therefore it has good utility for retrospectively diagnosing AMI Remember, CK-MB returns to baseline by 48 hours Troponin release can also be precipitated by other conditions that cause myocardial damage Troponin 20

21. to determine the effects of reperfusion, cTnT should be measured at the time of thrombolytic therapy initiation and 90 min. after therapy ▪ Troponin-I levels begin to rise 2-3 hours after onset of MI and roughly 80% of patients with AMI will have positive values at 3 hours ▪ Elevations in Troponin-I and Troponin-T can persist for up to 10 days after MI ▪ Therefore it has good utility for retrospectively diagnosing AMI ▪ Remember, CK-MB returns to baseline by 48 hours ▪ Troponin release can also be precipitated by other conditions that cause myocardial damage Troponin 21

22. other cardiac markers BNP and NT – pro BNP (Brain natriuretic peptide) To diagnose congestive heart failure To grade the severity of heart failure To differentiate between heart failure and lung disease To monitor the effects of therapy for heart failure 22

23. BNP (B type natriuretic peptide) It is a cardiac specific peptides first identified in porcine brain extracts and hence the name brain natriuretic peptide. BNP is a neurohormone released by ventricular myocardium in response to volume overload. Its primary utilization is for the 11/6/2021evaluation of patient with HF. It has shown to be a strong predictor of short and long-term mortality in patients with ACS. The clinical diagnostic cutoff level for heart failure is BNP LEVEL of >100 pg /mL 23

24. 24

25. Joe Smoker is an overweight 57-year-old white male who was cutting his grass when he experienced a sharp chest pain along with pain in his left arm. His wife rushed him to the hospital, fearing that he was having a heart attack. In the clinic, the physician examined Joe and sent him for electrocardiogram (ECG) and blood test for troponins, creatine kinase (CK), creatine kinase isoenzyme MB (CK-MB). Test results Reference Ranges Troponin I (ng/mL) 1.7 0.0–0.05 CK-MB (%) 7 <3.9 CK (IU/L) 275 46–171 25

26. Joe Returns About 6 months later, Joe is experiencing difficulty in breathing. His wife rushes him to the emergency department, fearing another heart attack. Blood test is sent to the laboratory with orders for cardiac markers B-type natriuretic peptide (BNP) assay is also ordered to check for heart versus pulmonary congestion. Test Results Reference Ranges CK-MB (%) 5 <3.9 CK total (IU/L) 183 46–171 Troponin I (ng/mL) 0.45 <0.5 BNP ( pg /mL) 185 <100* 26