Coronary Heart Disease, Vascular Diseases and HTN Atherosclerosis o Form of arteriosclerosis o Thickening and hardening is caused by accumulation

of lipid-laden macrophages in the arterial wall o Plaque development Pathophysiology of atherosclerosis o Accumulation of lipoproteins o Endothelial injury o Inflammation Atherosclerosis o Progression *Inflammation of endothelium *Cellular proliferation *Macrophage migration *LDL oxidation (foam cell formation) *Fatty streak *Fibrous plaque *Complicated plaque Non-atherosclerosis causes of cardiac ischemia o Embolus formation o Chest wall trauma o Coronary arterial dissection o Arteritis o Hematological disorders o Congenital coronary anomalies o Coronary artery spasm o Syndrome X (metabolic syndrome) o Increase in demand for myocardial O2 supply Coronary Artery Disease o Any vascular disorder that narrows or occludes the coronary arteries o Atherosclerosis is the most common cause o Modifiable Risk factors *Hyperlipidemia or dyslipidemia *Hypertension *Diabetes mellitus *Metabolic syndrome *Cigarette smoking *Obesity *Sedentary lifestyle
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*Excessive ETOH o Non-modifiable Risk Factors *Age *Male sex *Family history of premature CAD o Markers *Markers of inflammation and thrombosis *C-reactive protein, fibrinogen, protein C, and plasminogen activator inhibitor *Hyperhomocysteinemia *Elevated lipoprotein (a) *Coronary artery calcification detected by electron beam CT or multidetector CT *Pathophysiology of Myocardial Ischemia *When oxygen demands increase in the setting of limited oxygen supply, myocardial ischemia results *Regulation of coronary blood flow occurs at the level of the arterioles and is dependent on autonomic tone and an intact, functioning endothelium *Endothelial dysfunction secondary to atherosclerosis impairs the ability of the coronary arterioles to dilate when oxygen demands increase *Decreased coronary vasodilator reserve results in a supply-demand mismatch with resultant ischemia and the clinical pattern of angina o Consequences of myocardial ischemia *Severe and prolonged ischemia causes myocyte death, loss of contractile function and tissue infarction *In less severe ischemia, some myocytes remain viable but have depressed contractile function *Stunned myocardium *Hibernating myocardium o Clinical presentation of Myocardial ischemia *Local, temporary deprivation of the coronary blood supply *Stable angina *Variant angina *Prinzmetals angina *Silent ischemia *Sudden and extended obstruction of the myocardial blood supply *Acute coronary syndromes *Unstable angina, NSTEMI, STEMI *Myocardial infarction o Stable angina *Induced by physical exertion, exposure to cold, eating, emotional stress *Last 3-5 minutes *Relieved by rest or SL NTG *EKG

*Baseline often normal or non-specific ST segment/T wave changes *ST segment depression during angina *Abnormality * 70% luminal narrowing of 1 or more coronary arteries o Prinzmetals or variant angina *Angina without provocation, typically occurring at rest *EKG *Transient ST segment elevation during pain *Often associated AV block or ventricular arrhythmias *Abnormality *Coronary artery spasm o Silent Ischemia *Individuals may c/o only of fatigue, SOB, or feeling of unease. *More common in women. *Thought to be due to global or regional abnormality in LV sympathetic afferent innervation. *May occur in DM, following surgical denervation such as CABG or cardiac transplant or after local nerve injury from MI o Acute coronary syndromes *Unstable angina *Myocardial infarction *STEMI or non-STEMI o Unstable angina *Increase in angina frequency, severity or duration *Angina of new onset and or occurring at low level of activity or at rest *May not respond to SL NTG *EKG *Same as for stable angina, changes may be more pronounced *Occasional ST segment elevation during discomfort *Abnormality *Plaque rupture with platelet and fibrin thrombus, causing coronary obstruction *Myocardial infarction *Sudden and extended obstruction of the myocardial blood supply causing myocyte necrosis *Two major types *NSTEMI previously known as Subendocardial infarction or non-Q wave myocardial infarction *Occur as result of subtotal occlusive thrombus or a thrombus that initially totally occlusive but not sustained *Associated with ST segment depression or T wave inversion *STEMI or Transmural infarction
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*Results in severe cardiac dysfunction *Marked elevation of ST segment on EKG *MI can occur in various regions of the heart *Anterior, inferior, lateral, septal, posterior *Cellular injury *Cellular death *Structural and functional changes *Myocardial stunning *Hibernating myocardium *Myocardial remodeling *Repair o Clinical manifestations of MI *Sudden severe chest pain *Sensation of indigestion *N/V *Diaphoresis *Peripheral vasoconstriction o Evaluation of MI *History *PE *EKG (12 lead) Q waves and changes in ST segments and T wave *Serial cardiac enzymes alterations *Troponin I and troponin T most specific indicators of MI *Other enzymes: CK-MB and LDH1 isoenzymes o Right ventricular infarction *Usually occurs in association with inferior MI *Blood supply to both of these areas comes from right coronary artery *The presence of RV MI and inferior MI increases mortality *Clinical picture *Hypotension *Clear lungs *Prominent JVD *Evaluation *Right sided precordial EKG Complications of acute MI *Mechanical *Left ventricular failure *Right ventricular failure *Cardiogenic shock *Structure *Free wall rupture *Ventricular septal defect

*Papillary muscle rupture with acute mitral regurgitation *Electrical *Arrhythmias *Bradyarrhythmias *Ventricular ectopy *Tachyarrhythmias *Ventricular/Supraventricular *Sudden cardiac death *Conduction abnormalities *First, second and third degree heart blocks *Bundle branch blocks Lipids and vascular disease o Cholesterol reduction by means of diet, drugs, or surgery reduces the risk of CHD o For people at high risk for CHD, the lower the LDL-C the better the prognosis o Treatment with moderate doses of statins reduces the LDL-C by 30% to 40% beyond that achieved by diet Serum lipid levels LDL *Most strongly associated with development of CAD *For every 1% difference in LDL, there is a 2% to 3% difference in the risk for CAD *The LDL increases with: *Age and weight *Diets high in saturated fats and chol *Conditions such as hypothyroidism, nephrotic syndrome, liver disease *HDL *There is a strong inverse relationship between HDL and CAD *HDL < 40mg/dL is considered low *For every 1mg/dL decrease in HDL the relative risk factor for CAD increases 2% to 3% *HDL levels are affected by genetics, tobacco use, obesity, and physical activity *There are no clinical trials that indicate a decrease risk of CAD secondary only to increased HDL *Triglycerides *Life style modifications such as weight loss, dietary restriction, decreased alcohol consumption, smoking cessation, and increased physical activity decrease triglyceride levels *The reduction of triglycerides is considered the greatest risk reduction in patients with the highest risk (low HDL and high LDL) *The combination of high LDL, low HDL and high triglycerides places patients in the highest risk category for CAD
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Management of hyperlipidemia o Recommendations for cholesterol screening are from the National Cholesterol Education Program, the AHA. o Other associations, namely the American College of Physicians and the US Preventive Task Force disagree and recommend screening men age 35 to 65 and women age 45 to 65 o In screening programs, consider measuring serum total cholesterol at least once every 5 years in all adults 20 yrs of age and older o Measure serum cholesterol and HDL cholesterol in association with analysis of other risk factors for CHD o Consider measuring serum total chol in children who have a strong FH of high cholesterol or CHD o Do not screen patients who are acutely ill or pregnant o Do not use serum apolipoprotein studies or lipoprotein electrophoresis for general screening The serum total cholesterol is not significantly affected after a meal; therefore the screening can be done at any time the patient is seen. However, definitive measures should be drawn after a 12 to 14 hrs of fasting. Evaluate the test results o Serum total cholesterol o Adults *Desirable <200 mg/dL *Borderline 200-239 mg/dL *High > or = 240 mg/dL o Children and adolescents *Desirable <170 mg/dL *Borderline 170-199 mg/dL *High > or = 200 mg/dL o All elevated cholesterol levels should be confirmed by repeat measurement in 1 to 8 weeks and the average used for clinical decisions o A low serum cholesterol may be a sign of good health, proper diet and appropriate exercise or may signal disease. o LDL cholesterol *Adults *Desirable <130 mg/dL *Borderline risk 130-159 mg/dL *High risk >or =160 mg/dL *If the triglycerides are <400mg/dl, calculate LDL as follows: Total chol - HDL -(0.2 x triglycerides) o Triglycerides *Adults

*Desirable *Borderline *High *Very high

<150 mg/dL 200 to 400 mg/dL 400 to 1000 mg/dL >or = 1000 mg/dL

o It takes at least 4 to 6 weeks before lipid levels respond to dietary or drug therapy o If the LDL goal is achieved, monitor every 4 months and remeasure LDL yearly o More frequent monitoring of lipid levels is unnecessary in the absence of changes in dietary and/or drug therapy. Proposed Modifications to NCEP-ATP III Therapeutic Goals and Treatment Risk Category High CHD, CHD risk equivalent (10-y risk >20%) Moderately high > or = 2 Risk factors (10-y risk 10%-20%) Moderate > or = 2 (10-y risk <10%) Low (0-1 Risk factor) LDL-C Goal (mg/dL) <100 <70 * <130 <100 * <130 Initiate TLC (mg/dL) >or = 100 Consider Drug Therapy >or = 100 <100 * > or = 130 100 - 129 * > or = 160

> or = 130 > or = 130

<160

> or = 160

> or = 190 160-189 *

* Optional TLC = therapeutic life style changes Vascular Diseases and HTN *Peripheral arterial disease (PAD) *Atherosclerotic disease of the arteries that perfuse the limbs, especially the lower extremities *Classic symptoms *Intermittent claudication due to exertion and relieved by rest *PE findings *Absent or diminished pulses distal to the stenosis *Bruit over the disease arteries *Hair loss *Thin shiny skin
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*Muscle atrophy *Risk factors *Smoking, HTN, DM, Hyperlipidemia *Evaluation *Ankle-brachial index (ABI) less than 0.9 *Normal ABI 0.9 to 1.3 *Sensitivity and specificity 95% and 99% *Duplex US *Angiography *Medical treatment *Lifestyle and risk factor modification *Antiplatelet therapy Aneurysm o Aortic aneurysm *Local dilation or outpouching of a vessel wall *True aneurysms *Fusiform aneurysms *Circumferential aneurysms *False aneurysms *Saccular aneurysms *Abdominal aortic aneurysm is common in older adults *Thoracic aortic aneurysm is less prevalent *Major risk factors *Age *Cigarette smoking *HTN *Family hx of aortic aneurysm *Atherosclerosis *Other risk factors *Marfan syndrome, Ehlers-Danlos syndrome, vasculitis with connective tissue disease, chronic infection, trauma *Most patients are asymptomatic *Some develop vascular complications *Expansion of aneurysm and compression of adjacent structures *Formation of thrombi with occlusion of distal segments *Classic physical finding is pulsatile non-tender mass below the umbilicus *Hypotension and acute abdominal pain may be due to aneurysm rupture (medical emergency) *Diagnosis by duplex US o Aortic dissection *Intima layer is torn from the aortic wall leading to formation of false lumen parallel to the true lumen *Risk factors *HTN

*Cocaine use *Trauma * Hereditary connective tissue diseases *Vasculitis *Bicuspid aortic valve *Coartation of the aorta *Symptoms include acute onset of severe chest or back pain, abdominal pain, syncope, and stroke o Other arterial diseases *Thromboangiitis obliterans (Buerger disease) *Occurs mainly in young men who smoke *Inflammatory disease of peripheral arteries resulting in the formation of nonatherosclerotic lesions *Obliterates the small and medium-sized arteries *Causes pain, tenderness, and hair loss in the affected area *Symptoms are caused by slow, sluggish blood flow *Can often lead to gangrenous lesions *Raynaud phenomenon and Raynaud disease *Episodic vasospasm in arteries and arterioles of the fingers, less commonly the toes *Raynaud disease is a primary vasospastic disorder of unknown origin *Raynaud phenomenon is secondary to other systemic diseases or conditions Pulmonary vascular disease o Pulmonary arterial hypertension *Caused by combination of pulmonary vasoconstriction, endothelial cell and/or smooth muscle proliferation, intimal fibrosis, and thrombosis in the pulmonary capillaries and arterioles *Primary is idiopathic *Secondary due to connective tissue disease, congenital heart disease, portal HTN, HIV infection, or drugs *Patients with mild disease are asymptomatic, those with severe disease c/o dyspnea, CP, syncope o Pulmonary arterial hypertension *Physical findings *Left parasternal lift *Loud pulmonary component of S2 *Murmur of tricuspid or pulmonic regurgitation *Hepatosplenomegaly (HSM) *Peripheral edema or ascites *Associated EKG abnormalities *RVH, left atrial enlargement, right axis deviation *Diagnosis *Echocardiogram
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Venous thromboembolic disease o Deep vein thrombosis *Obstruction of venous flow leading to increased venous pressure *Factors *Venous stasis *Venous endothelial damage *Hypercoagulable states *Symptoms *Pain and swelling *Some patients are asymptomatic *Patients with upper extremity DVT can develop superior vena cava syndrome *PE *Tenderness, erythema, warmth, and swelling below the site of thrombosis. Homans sign has low sensitivity and specificity *Evaluation *D-dimers *Duplex US o Pulmonary embolism *Occurs when a thrombus dislodges from the deep veins of the upper or lower extremities *Pulmonary artery resistance increases due to *Anatomic reduction in cross sectional of the pulmonary vascular bed *Functional hypoxia-induced pulmonary vasoconstricition *The pressure overload in the right ventricle can lead to dilation, hypokinesis, and tricuspid regurgitation *Affected areas of lung tissue are ventilated but not perfused, this causes arterial hypoxemia *Classic symptoms of acute PE *Sudden onset of dyspnea, and pleuritic chest pain *Other symptoms: anginal CP, hemoptysis, syncope *Physical findings *Tachypnea and tachycardia *Additional findings: right ventricular lift, inspiratory crackles, loud pulmonary component of S2, expiratory wheezing, and pleural rub *Diagnosis *ABGs: hypoxemia, respiratory alkalosis, and high alveolar to arterial O2 tension gradient *EKG: most common ST. less common AF, PAC, SVT. New RBBB or right axis deviation and P wave pulmonale *VQ scan less than 10% are interpreted as normal *Spiral CT more accurate o Venous thromboembolism prophylaxis *Patients at risk for VTE should receive prophylaxis with heparin *Patients at risk include: hospitalized with acute medical illnesses (CHF, acute respiratory illnesses, acute inflammatory disease) or those in prolonged BR (>3

days) *Mechanical prophylaxis with intermittent pneumonic compression Arterial hypertension o Hypertension *Primary hypertension *Essential or idiopathic hypertension *Genetic and environmental factors *Affects 92% to 95% of individuals with hypertension o Secondary hypertension *Caused by a systemic disease process that raises peripheral vascular resistance or cardiac output o Isolated systolic hypertension *Elevations of systolic pressure are caused by increases in cardiac output, total peripheral vascular resistance, or both o Complicated hypertension *Chronic hypertensive damage to the walls of systemic blood vessels *Smooth muscle cells undergo hypertrophy and hyperplasia with fibrosis of the tunica intima and media o Malignant hypertension *Rapidly progressive hypertension *Diastolic pressure is usually >140 mm Hg *Clinical picture: *BP > 220/140 mmHg *HA, confusion, blurred vision, N/V, seizures, heart failure, oliguria, retinopathy o Initial evaluation goals *Accurate assessment of blood pressure *Based on average of 2 separate readings taken at two or more office visits *Assessing the patients overall cardiovascular risks *Hypercholesterolemia, smoking, DM *Detecting clues of secondary hypertension Classification of Blood Pressure per JNC VII
BP Classificatio n Normal Prehypertension Stage 1 SBP (mmHg) DBP (mmHg) LSM

<120 120-39

and <80 or 80-89

Encourage Yes

140-159

or 90-99 11

Yes

Hypertension Stage 2 hypertension BP= blood pressure 160 or 100 Yes LSM= Life

SBP= Systolic BP DSP= Diastolic BP Style Modifications

o Secondary causes of HTN *Chronic kidney disease most common cause *Mechanisms of HTN due to expanded fluid volume and peripheral vasoconstriction *Renal artery stenosis *Main causes include atherosclerosis *Primary aldosteronism *Unilateral aldosterone producing adenoma *Bilateral adrenal hyperplasia *Mendelian forms of HTN *Rare inherited traits *HTN is caused by excessive activation of epithelial Na+ channel which causes excessive reabsorption of Na+ from the distal nephron *Pheochromocytoma *Rare catecholamine producing tumor of the adrenal glands o Hypertension in African Americans *Disproportionate number affected *Environmental factors have main role *High dose ACE inhibitor plus diuretic effective o Hypertension in diabetics *HTN present in 75% of diabetics *Major factor contributing to risk of MI, stroke, HF, microvascular complications and diabetic nephropathy progressing to ESRD *BP should be lowered to < 130/80 *Typically requires 3-5 drugs. ACE or ARB are first choice o Hypertension in patients with CAD *To lower myocardial O2 demands, BP should be reduced without causing reflex tachycardia * blocker in conjunction with dyhydropyridine CCB * blocker is indicated for patients who have suffered an MI and most patients with chronic heart failure *ACE inhibitors are indicated for patients with left ventricular systolic dysfunction and sometimes used in patients after an MI without ventricular dysfunction o Isolated systolic HTN in older adults

*Systolic pressure rises with age, diastolic pressure rises until age 50 then decreases, causing rise in PP *Primary cause is decreased distensibility of the large arteries *Collagen replaces elastin in the aorta, an age dependent process accelerated by atherosclerosis and HTN *Cardiovascular risk is related to pulsatility (pounding of the blood vessels and more rapid return of the arterial pulse wave from the periphery), which further increases systolic HTN *Majority of patients with uncontrolled HTN, have isolated systolic HTN o Hypertensive disorders of women *Hormones *Pre-Eclampsia o Resistant HTN *Defined as BP > 140/90 despite full doses of 3 or more meds *Pseudoresistance *Inadequate medical regime *Non-adherence or ingestion of pressor substances *Secondary HTN

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