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Contents Arteriosclerosis Tumors of blood vessels Heart failure Ischemic heart disease Sakchai Chitpakdee, M.D. Valvular heart diseases Rheumatic heart disease Infective endocarditis Myocarditis Pericardial diseases Arteriosclerosis = hardening of the arteries y Atherosclerosis ○ Large & medium size vessels y Monckeberg medial calcific sclerosis ○ Medium size vessels with tunica media calcification y Arteriolosclerosis ○ Small arteries/arterioles Atherosclerosis “intimal lesion”: atheromas or fibrofatty plaques or atheromatous plaques” Large and medium size arteries y Raised focal plaque within the intima y Core lipid (cholesterol/cholesterol esters) and a covering fibrous cap y Cells: foamy cells (macrophage/SMC), lymphocytes Atherosclerosis Complicated lesion: y Calcification y Rupture/ulceration -> atheroemboli, thrombus y Hemorrhage y Thrombosis y Aneurysmal dilation Atherosclerosis Epidemiology & risk factors: y Age: middle or later age y Sex: pre-menopause -> M > F 60s to 70s -> M = F y Genetics: familial y Hyperlipidemia: high cholesterol/TG & ↓ HDL y Hypertension y Cigarette smoking y Diabetes mellitus Atherosclerosis Clinical features & prevention Epidemiology & risk factors: Clinical features: y Elevated plasma homocysteine y Ischemic/infarction of organs y Other factors: y Atherosclerotic aneurysm ○ Competitive stressful lifestyle: type A personality Prevention: ○ Lack of exercise y Primary prevention: risk factor modification ○ Obesity y Secondary prevention: prevent recurrence of y Moderate intake of alcohol -> protective events or complications (antiplatlet drugs etc) factor Tumors Tumors Benign neoplasms: Intermediate-grade neoplasms: y Hemangioma: capillary, cavernous, pyogenic y Kaposi sarcoma granuloma y Hemangioendothelioma y Lymphangioma: simple (capillary), cavernous lymphangioma (cystic hygroma) Malignant neoplasms: y Glomus tumor, myopericytoma y Angiosarcoma y Vascular ectasia: nevus flammeus, spider y Hemangiopericytoma (benign & malignant) telangiectasia, hereditary hemorrhagic telangiectasia (osler-Weber-Rendu dis.) y Bacillary angiomatosis: B. henselae infection Hemangioma Hemangioma Pyogenic granuloma (lobular capillary) Capillary hemangioma: y Polypoid nodules of skin, gingiva, oral y Skin, subcutaneous tissue, oral cavities of head mucosa and neck, lung, liver, kidney y Bleeding, ulcerated y Strawberry type (juvenile hemangioma): 1:200 y Granuloma gravidarum: 1% pregnant newborns: fade 1-3 yr, regress by 7 yr women, pyogenic granuloma at gingiva, Cavernous hemangioma: regress after delivery y Older age, less circumscribed, deeper y No regress Lymphangioma Lymphangioma circumscriptum (capillary ymphangioma) y Subcutaneous mass of head and neck Cavernous lymphangioma y Cystic hygroma y Neck and axilla of children y Turner syndrome: neck region Vascular ectasia Kaposi sarcoma Nevus flammeus: Chronic, classic european KS y Birthmark of head and neck, flat Lymphadenopathy, African, endemic KS y Pink to purple Æ regress Transplant-associated Port-wine stain: no regress (immunosuppression-associated) KS y Trigeminal nerve Æ Sturge-Weber syndrome (ecephalotrigemina AIDS-associated KS angiomatosis), venous mass of Clinical: patchesÆ plaquesÆ nodules leptimeninges Æ seizure, hemiplegia, mental retardation Cause: HSV-8, HIV? Angiosarcoma Malignant endothelial neoplasms Skin, soft tissue, breast, liver Cause: y Breast: radiation, lymphedema y Liver: polyvinyl chloride (PVC), throrotrast y Skin: arsenic (pesticide) Heart failure Left-side heart failure Cause: IHD, HT, aortic & mitral valve CHF = congestive heart failure disease, cardiomyopathy Common end result of many forms of HD Clinical: Unable to pump blood at rate of body y Forward effect: poor organ perfusion requirement (prerenal azotemia, hypoxic Progressive deterioration of myocardial encephalopathy) contraction y Backward effect: pulmonary edema y Systolic dysfunction (dyspnea, orthopnea, PND) y Diastolic dysfunction Right-side heart failure What is Ischemic Heart Disease? Cause: pulmonary HT (cor pulmonale) Myocardial ischemia Hypertrophy of right ventricle, atrium, Imbalance btw supply (perfusion) & demand of septum Æ left-side HF oxygenated blood Clinical: Ischemia Æ ↓Oxygen y Forward effect: poor oxygenation Æ ↓ Nutrient substrates y Backward effect: organ edema, effusion Æ ↓ Metabolites removal Ischemia Æ Dysfunction of pumping Æ Abnormal heart rhythms Æ Myocardial infarction (Necrosis) Etiology of IHD Clinical manifestation 90 % Æ coronary artery Four syndromes: atherosclerosis 1. Myocardial infarction 2. Angina pectoris: variants y Atherosclerosis Æ narrow lumen 1. Stable angina Æ thrombus formation 2. Prinzmetal angina Æ coronary vasospasm 3. Unstable angina 3. Chronic ischemic heart disease Others: hypertrophy, hypovolemia, 4. Sudden cardiac death hypoxemia,↑ heart rate Clinical manifestation Role of fixed coronary obstruction At least 75 % reduction of cross- Stable plaque Æ Unstable plaque sectional area (insufficient compensatory Stable angina Æ Acute coronary vasolidation) syndromes At least 90 % reduction Æ ischemia at rest Acute coronary syndromes: Atherosclerosis type IV-VI unstable angina, acute MI, and Affected location: proximal (LAD, LCX), sudden death entire (RCA) Role of acute plaque change Acute plaque change/disruption: y Hemorrhage into atheroma Æ ↑ volume y Rupture or fissuring Æ Thrombosis y Erosion or ulceration Æ Thrombosis A = Plaque rupture B = Thrombus over plaque rupture C = Massive plaque rupture with thrombus Angina pectoris Angina pectoris Paroxysmal and usually recurrent attacks of Stable angina: substernal or precordial chest discomfort caused by y Most common, and predictable transient (15 sec to 15 min) myocardial ischemia y Reduction of coronary perfusion by chronic that falls short of inducing cellular necrosis (infarct) stenosing coronary atherosclerosis Three patterns: y Pain brought by physical excertion, emotional y Stable or typical angina stress, heat or cold fever, anemia etc y Prinzmetal or variant angina y Pain relieved by rest (decreased demand) or y Unstable or crescendo or accelerating or nitroglycerin (vasodilator) preinfarction angina y Monitoring ECG: ST segment depression or elevation or T-wave inversion Angina pectoris Angina pectoris Prinzmetal variant angina: Unstable angina: y Uncommon, and unpredictable y Angina occurring with increasing frequency, y Occur at rest not related to physical and emotional precipitated with less effort, often occurs at exertion rest and tends to be prolonged duration y Coronary artery vasospasm y Most induced by disruption of atherosclerotic plaque with partial thrombosis and possibly y Atherosclerosis-induced hypercontractility, embolization or vasospasm vasospastic chemicals secretion by mast cells and abnormal calcium influx y Harbinger of subsequent acute MI y Response well to calcium-channel blockers and y Thrombus labile and lasts 20 to 30 minutes nitroglycerin y 10 to 15% total occlusion Å collateral vessel y ECG: elevation of ST-segment Myocardial infarction Myocardial infarction Necrosis of myocardium Transmural (Q-wave) infarction Prolonged period of ischemia at rest lasting > y Full or nearly full thickness necrosis 20 min, unresponsive to NTG y Acute plaque change + completely obstructive Ischemic ECG change and positive cardiac thrombosis (fixed and persist > 1 hour) enzymes y ECG: ST segment elevation Æ Q wave Subendocardial (Non-Q-wave) infarction 25 % silent: old age, diabetics y 1/3 to ½ inner ventricle thickness necrosis Subendocardial VS Transmural infarction y Incomplete obstructive thrombosis (>30-40 min) y Non-Q-wave VS Q-wave infarction y ¼ complete obstruction + collateral supply y ECG: ST segment elevation Æ Non-Q-wave Morphological change Almost all transmural MI involve at least a portion of left ventricle Coronary arteries and MI site: y LAD (40-50%) -> ant wall of LV, apex, ant portion of ventricular septum y RCA (30-40%) -> inf-post wall of LV, post portion of ventricular septum, RV (inf-post) y LCX (10-20%) -> lateral wall LV except apex 1 day 3 to 4 days 7 to 10 days 3 weeks Evolution of morphology change Cardiac enzymes Time Morphology change 0 - ½ hours Ultrastructural change (EM) Released enzymes after myocardial cell 2 – 3 hours Triphenyltetrazolium chloride dye: dead: noninfarct area Æ brick-red, infarcted Æ unstained y Myoglobin 4 – 24 hours Gross: dark mottling area, y Troponin (TnI and TnT) Histology: hemorrhage and necrosis y Creatine kinase (total CK and CK-MB) 1 – 7 days Gross: yellow-tan mottling, reddish border Histology: neutrophils and macrophages y LDH (LDH1, LDH2) 7 – 14 days Gross: red-tan margin Histology: macrophages and granulation tissue 2 – 8 weeks Gross: gray-white scar Histology: collagen deposition > 2 months Scarring complete Cardiac enzymes Consequences and complications 7x Myoglobin 6x Total CK 50 % AMI Æ dead Half of dead occur within 1 hour (VF) 5x In-hospital death rate 30% Æ 10-13 % 4x 75 % develop one or more complications LDH 3x y Contractile dysfunction Æ cardiogenic shock 10 – 15 % of AMI and 70 % mortality rate 2x CK-MB Troponin I y Arrhythmias Æ sudden death Upper limit of normal serum level of normal limit Upper 1x bradycardia, tachycardia, VPC, VT, VF asystole 0 20 40 60 80 100 120 140 160 Hours from onset of infarction Consequences and complications Consequences and complications Ventricular aneurysm Æ thrombus, Myocardial rupture: arrhythmias, heart failure, rupture y Ventricular free wall Æ cardiac
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  • Prehypertension Increases the Risk for Renal Arteriosclerosis in Autopsies: the Hisayama Study

    Prehypertension Increases the Risk for Renal Arteriosclerosis in Autopsies: the Hisayama Study

    JASN Express. Published on June 20, 2007 as doi: 10.1681/ASN.2007010067 CLINICAL EPIDEMIOLOGY www.jasn.org Prehypertension Increases the Risk for Renal Arteriosclerosis in Autopsies: The Hisayama Study Toshiharu Ninomiya,* Michiaki Kubo,* Yasufumi Doi,† Koji Yonemoto,* Yumihiro Tanizaki,* Kazuhiko Tsuruya,† Katsuo Sueishi,‡ Masazumi Tsuneyoshi,§ Mitsuo Iida,† and Yutaka Kiyohara* Departments of *Environmental Medicine, †Medicine and Clinical Science, ‡Pathophysiological and Experimental Pathology, and §Anatomic Pathology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan ABSTRACT Information regarding the association between prehypertension BP level and renal arteriosclerosis is limited. In 652 consecutive population-based autopsy samples without hypertension treatment before death, the relationship between the severity of renal arteriosclerosis and BP levels classified according to the criteria of the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure was examined. The age- and gender-adjusted frequencies of renal arteriosclerosis linearly increased with elevating BP levels; both hypertensive and prehypertensive subjects had significantly higher frequencies of renal arteriosclerosis than subjects with normal BP (normal 11.9%; prehypertension 28.5%; stage 1 hypertension 32.9%; stage 2 hypertension 58.2%; all P Ͻ 0.01 versus normal). In a logistic regression model, prehypertension was significantly associated with renal arteriosclerosis after adjustment for other cardiovascular risk factors (prehyper- tension multivariate-adjusted odds ratio [mOR] 5.99 [95% confidence interval (CI) 2.20 to 15.97]; stage 1 hypertension mOR 6.99 [95% CI 2.61 to 18.72]; stage 2 hypertension mOR 22.21 [95% CI 8.35 to 59.08]). This significant association was observed for all renal arterial sizes.