Valvular diseases Myocardial diseases Congenital heart diseases Diseases of the pericardium Cardiac neoplasms
HYPERTROPHY OF THE HEART AND HEART FAILURE Normal values Weight: women: 300 gs, men: 350 gs Free wall thickness: RV: 3-4 mm, LV:10-11 mm End-diastolic volume (EDV) 120 ml, end-systolic volume (ESV) 50 ml, stroke volume (SV) 70 ml Hypertrophy of the heart The cardiac myocytes are permanent cells (not able to enter the cell cycle) and, therefore, are not able to proliferate Increase in work load increase in size and pumping capacity of ventricular myocytes Weight > 400 g Types: concentric or dilative Concentric hypertrophy Pathogenesis An obstruction of outflow in systole (i.e., hypertension, aortic valve stenosis) the LV increases the end-systolic pressure pressure overload concentric remodeling and hypertrophy Morphology Concentric hypertrophy of the LV: small lumen; markedly increased wall thickness (> 20 mm); increased mass (> 500 g) Clinical features of pressure-overloaded LV Symptomless for a long period Pump failure occurs lately Risk of sudden cardiac death Dilative hypertrophy Pathogenesis In diastolic backflow because of aortic/mitral valve incompetence the regurgitated extra volume of blood is accepted with the dilation of the LV an increased EDV is ejected into the circulation during the next systole (volume overload) excentric remodeling and hypertrophy Morphology Dilative hypertrophy of LV: enlarged lumen, enlarged size, slightly increased wall thickness, increased mass Clinical features of volume-overloaded LV Pump failure occurs relatively early Good response to drugs increasing contractility The overall prognosis is better than that of pressure-overloaded heart Cardiac hypertrophy (HT) culminates in congestive heart failure Hypertension or aortic stenosis-induced pressure overload concentric HT Noncontracting areas in myocardial infarction lead to volume overload dilative HT Aortic or mitral incompetence-induced volume overload dilative HT These conditions lead to increased cardiac work increased wall stress increased cell strech progressive dilative hypertrophy decreased contractility (systolic dysfunction) Neurohumoral activation occurs: increased secretion of atrial natriuretic peptide and norepinephrin, activation of the renin-angiotensin-aldosteron system Pump failure, arrhythmias death ARRHYTHMIAS Two types: tachyarrhythmia (>100 beats/minute) and bradyarrhythmia (
