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| ===Dynamic Left Ventricular Outflow Obstruction (LVOTO)=== | | ===Dynamic Left Ventricular Outflow Obstruction (LVOTO)=== |
− | This may be caused by systolic anterior motion of the mitral valve (SAM) and mid-systolic contact of the left ventricular free wall (LVFW) with the interventricular septum (IVS) during systole. | + | This may be caused by systolic anterior motion of the mitral valve (SAM) and mid-systolic contact of the left ventricular free wall (LVFW) with the interventricular septum (IVS) during systole - cavity obliteration. |
| ====Systolic Anterior Motion of the Mitral Valve (SAM)==== | | ====Systolic Anterior Motion of the Mitral Valve (SAM)==== |
| This is where the anterior mitral valve leaflet moves towards the IVS in systole, therefore creating obstruction in the left ventricular outflow tract which interferes with the LV outflow in mid-systole. As a result of this movement, the mitral valve leaflet does not completely seal the atrioventricular annulus; this causes a secondary mitral regurgitation. The combination of turbulent blood flow in the left ventricular outflow tract and mitral regurgitation causes a systolic murmur which can be identified on auscultation. | | This is where the anterior mitral valve leaflet moves towards the IVS in systole, therefore creating obstruction in the left ventricular outflow tract which interferes with the LV outflow in mid-systole. As a result of this movement, the mitral valve leaflet does not completely seal the atrioventricular annulus; this causes a secondary mitral regurgitation. The combination of turbulent blood flow in the left ventricular outflow tract and mitral regurgitation causes a systolic murmur which can be identified on auscultation. |
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| + | The mechanism of SAM is not completely understood. One hypothesis is that deformation of the mitral valve architecture (leaflets, chordae tendinae, papillary muscles) and the hyperdynamic state caused by myocardial hypertrophy cause SAM. |
| + | ===Diastolic Dysfunction=== |
| + | Myocardial hypertrophy and interstitial fibrosis leads to reduced LV compliance. Tachycardia can exacerbate diastolic dysfunction by reducing diastolic time, and hence the time allowed for ventricular filling. Since coronary blood flow to supply the myocardium occurs in diastole, tachycardia may accelerate myocardial ischaemia. Diastolic dysfunction causes increased LV filling pressure. Left atrial (LA) enlargement initially compensates for this until maximal compliance of the atrium is reached. Once this point is reached, atrial pressure rises. This will subsequently result in pulmonary venous hypertension and eventually left-sided congestive heart failure. SAM and mitral regurgitation further contribute to ventricular filling pressure. |
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| + | ===Systolic Dysfunction=== |
| + | Systolic dysfunction can be a feature of any myocardial disease in which there is significant ischaemia and replacement fibrosis of the myocardium. This results in reduced stroke volume and increased ventricular filling pressure. |
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| ==Clinical Signs== | | ==Clinical Signs== |
| + | A large proportion of cats with HCM are asymptomatic, and diagnosed as a result of echocardiography for investigation of a murmur or gallop rhythm detected on auscultation. A murmur is present in >50% of cats with HCM, due to dynamic left ventricular outflow tract obstruction and mitral regurgitation caused by SAM of the mitral valve. |
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| ==Diagnosis== | | ==Diagnosis== |
| ===Genetic Testing=== | | ===Genetic Testing=== |
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| ==Treatment== | | ==Treatment== |
| ==Prognosis== | | ==Prognosis== |
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| + | [[Category:Cardiology Section]] |