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HCM: Symtomps: Angina, Dyspne, Presyncope, Syncope. Physical Findings:

HYPERTROPHIC CARDIOMYOPATHY: Cellular changes of myocytes . Cell disarrangement ise seen on microscope . Left : Organized and parallel cell arrangement in normal myocardium . Right : Disarrangement affects impuls conduction and promotes ventricular arrythmias. HCM:

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HCM: Symtomps: Angina, Dyspne, Presyncope, Syncope. Physical Findings:

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  1. HYPERTROPHIC CARDIOMYOPATHY: Cellularchanges of myocytes. Celldisarrangement ise seen on microscope. Left:Organizedandparallelcellarrangement in normal myocardium. Right:Disarrangementaffectsimpulsconductionandpromotesventriculararrythmias.

  2. HCM: Symtomps:Angina, Dyspne, Presyncope, Syncope. Physical Findings: • 1- Before LV beat, LA beat is palpated (S4): Is present even in the absence of any gradient or murmur. Impaired LV relaxation. • 2- LVOT Sistolik ejectıon Murmur: Crescendo-Decrescendo, starts with S1 and ends with S2. Best heard between apex and left sternal border. Cervical radiation is weak. Augmented by manouvers and drugs which decrease preload. (Valsalva, standing, amyl nitrite). Attenuates with increasing afterload (squating, handgrip fenilefrin). • 3- MR murmur: Heard at late systole, radiates to axilla, and related with LV outflow obstruction. Mitral diastolic rumble and Paradoxic splitting of S2 may be heard. • 4- Hyperdynamic carotis pulse.

  3. HCM: Clinical Presentation and Mechanisms • Chest pain: Ischemia, LVOT ob. Reduced coronary perfusion pressure. • Exertional dyspnea: Diastolic dysfunction. • Reduced functional capacity: LVOTob, systolic dysfunction, AFwith uncontrolled rapid ventricular rate. • Palpitation: SVT, AF, frequent VPB, non-sustained VT. • Syncope/Presyncope: Supraventricular arrythmia, LVOTob, vasovagal, high VT rate . İnadequate increase cardiac output during the effort. • Cardiac arrest: VT, SVT, AF, VF, bradyarrythmia.

  4. HCM: Other manifestations. Atrial Fibrillation • Seen in %15 of patients with HCM. • Absence of atrial systole. Rapid ventricular rate causes pulmonary edema or hypotension. • Rapid ventricular rate causes detoriation of functional capacity. • By conversion to sinus rythm or decreasing heart rate functional capacity improves. Endocarditis: May occur on aortic or mitral valves. Unexpected heart failure and IE symptoms or signs should be suggest İE in HCM patiernts.

  5. HCM: ECG and CHEST FİLM Chest film: May be normal-large left heart chambers. . No aortic calcification. ECG: Is anormal in %97 of symptomatic HCMP, and in %90 of asymptomatic HCMP patients. • AF is detected in %15. • Non-sustained VT is frequent. . • Q waves in DII, DIII, aVF and D1, aVL, V5, V6 (and less frequently in V1-3). This sign shows hypertrophy, and causes pseudoinfarct patern. • Intraventricular conduction delay. High voltage findings of LVH. T waves of LVH. Huge negative T waves are frequently seen in apical HCMP high precordial QRS voltage. • Short PR and pre-exitation may be seen, but is infrequent.

  6. HCM: Characteristic ECG paterns. • Left axis deviation • LBBB • Pathologic Q wave on anterolateral leads. • T wave inversion (commonly in İnferolateral leads) • ST segment changes. • Criteria for left atrial enlargement. • V3-5 or V4-6 huge T wave inversion (“Distal- apikal HCM”

  7. HCM: Pseudoinfarction patern, Q wave.

  8. HCMP: Echocardiographic Hallmarks • Asymetric (dispropotionate) septal thickening: Septum to posterior wall ratio > 1.5 • LV myocardial segment >1.5 cm in thicknesss. • Poor Septal contractıon. Hypercontractile free posterior wall. • Systolic anterior motıon of the mitral valve (SAM) when outflow tract gradient >30 mmHg . • Mid-systolic closure of aortic valve. • Small LV cavity. • Mitral regurgitation is frequent. • LVOT gradient at rest present in about %35 of patients

  9. Hypertrophic obstructive cardiomyopathy (HOCM): AsMitral valve changes:When the LVOTis narrowed, blood rushes through the passageway toward the aortic valve dragging the leaflets of the mitral valve with it. Mitral valve normally functıons keep blood floıwing in direction from the left atrium (upper heart chamber) to the LV. However increased force of blood caused by HCM pulls the valve open and may cause blood leak backward (called regurgitatıon )into the LA. NORMAL LVOTobs.

  10. Anterıor replacement of the papillary muscle in HOCM : MR, Systolic anterior motion (SAM)

  11. HCM vs Athlete’s Heart HCM Athlete + Unusual pattern of LVH -+ LV cavity <45 mm -- LV cavity >55 mm ++ LA enlargement -+ Bizarre ECG paterns -+ Abnormal LV filling -+ Female gender --  thickness with deconditioning ++ Family history of HCM - Circulation 1995; 91:1596

  12. HOCM: Septal myectomy: Before the operatıon There is severe hypertrophy of the basal septum, whith systolic anterior motıon of the mitral valve (-A-). This results in severe LVOT obs. as well as MR. During the surgery (-B ), yhe portıon of the basal septum that project into the outflow tract is removed by scalpel, resulting in abolitıon of the LVOTobs. (-C-). There is no longer SAM, and theMR abolished.

  13. HOCM:Septal ablation (with absolute ethanol). İndication: LVOT gradient at rest > 30-50 mmHg. With provocation 75-100 mmHg.

  14. HOCM:Decreased LVOT gradient after septal ablation.

  15. Restictive Cardiomyopathy

  16. Tanım: Ventriküler sertliğin daha farklı mekanizma/patolojilerle artış gösterdiği bir grup bozukluğu temsil etmektedir. İnfiltrtif , inflamatuar veya metabolik hastalıkların sonucunda restriktif kardiyomyopati gelişebilir.

  17. Idiopathic Dilated Cardiomyopathy

  18. IDC - Definition • a disease of unknown etiology that principally affects the myocardium • LV dilatation and systolic dysfunction • pathology • increased heart size and weight • ventricular dilatation, normal wall thickness • heart dysfunction out of portion to fibrosis

  19. Incidence and Prognosis • 3-10 cases per 100,000 • 20,000 new cases per year in the U.S.A. • death from progressive pump failure1-year 25% 2-year 35-40% 5-year 40-80% • stabilization observed in 20-50% of patient • complete recovery is rare

  20. Observed Survival of 104 Patients Years Am J Cardiol 1981; 47:525

  21. Predicting Prognosis in IDC Predictive Possible Not Predictive Clinical factors symptoms alcoholism age peripartum duration family history viral illness Hemodynamics LVEF LV size Cardiac index atrial pressure Dysarrhythmia LV cond delay AV block simple VPC complex VPC atrial fibrillation Histology myofibril volume other findings Neuroendocrine hyponatremia plasma norepinephrine atrial natriuretic factor

  22. Clinical Manifestations • Highest incidence in middle age • blacks 2x more frequent than whites • men 3x more frequent than women • symptoms may be gradual in onset • acute presentation • misdiagnosed as viral URI in young adults • uncommon to find specific myocardial disease on endomyocardial biopsy

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