Michaela
Savannah Super Cat
Thus is the non translated medical repost in Romeo still asymptomatic at this time -
No time to translate to normal non medical language yet.
So here I am with my second cat with HCM . Most pet owner will not detect a murmur or spend the $$$ on a asymptomatic kitten .
Like the breeder saids " what is the big deal if he is asymptomatic"
The big deal is sudden death and irreversible clot and heart failure like my 9 y old cat had .....
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ECHOCARDIOGRAPHIC FINDINGS: The patient was not sedated and imaged well. Subjectively, the right heart is normal. The diameter of the main pulmonary artery is within normal limits. Transpulmonary flow velocities within normal limits. There is moderate (0.8-0.9 IVSd) regional LV hypertrophy. There is Doppler and m-mode evidence of left ventricular outflow tract obstruction with little
evidence of mitral regurgitation. The left atrium is mildly enlarged (1.8 cm) with normal auricular emptying velocities. The transmitral flow velocity profile documents E/A reversal consistent with a relaxation abnormality. There is no evidence of pericardial effusion or a cardiac mass lesion. DIAGNOSTIC INTERPRETATION: Today's evaluation is consistent with a diagnosis of hypertrophic obstructive cardio myopathy with moderate hypertrophy and mild left atrial enlargement. There is no evidence of an intra-cavitary thrombus or sontaneous echocardiographic contrast. CLINICAL ASSESSMENT: Today's examination is consistent with a diagnosis of hypertrophic obstructive cardiomyopathy. The degree of hypertrophy coupled with the patient's young age 9 mo. makes me concerned about the long-term prognosis. I believe the severity of the changes places this patient at substantially increased risk for anesthetic complications. I do not recommend general anesthesia unless absolutely necessary. I believe it is reasonable to adopt either an aggressive or conservative appro management would include initiation of the beta blocker (atenolol) at a dose of 1 mg/kg orally twice daily, with gradual up titration to consistently obtain a target heart rate of approximately 130-140 bpm. Additionally, administration of a platelet aggregation inhibitor (clopidogrel or aspirin) could be considered. The mild left atrial enlargement, coupled with the normal auricular emptying velocities suggest that this patient is probably not at markedly increased risk for thromboembolic events however accurate prediction of the risk of these events is challenging. I've placed a call to Dr. Kate Meurs at North Carolina State University to inquire into whether or not she has identified specific genetic mutations in this breed and associated them with early development of hypertrophic cardiomyopathy. Submitting blood to her lab may prove informative. Repeating the echocardiogram in 4-6 months should provide important prognostic information. This reevaluation should be performed whether medical management is started or not.
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Sent from my iPhone using Tapatalk
Michaela L
No time to translate to normal non medical language yet.
So here I am with my second cat with HCM . Most pet owner will not detect a murmur or spend the $$$ on a asymptomatic kitten .
Like the breeder saids " what is the big deal if he is asymptomatic"
The big deal is sudden death and irreversible clot and heart failure like my 9 y old cat had .....
=========================
ECHOCARDIOGRAPHIC FINDINGS: The patient was not sedated and imaged well. Subjectively, the right heart is normal. The diameter of the main pulmonary artery is within normal limits. Transpulmonary flow velocities within normal limits. There is moderate (0.8-0.9 IVSd) regional LV hypertrophy. There is Doppler and m-mode evidence of left ventricular outflow tract obstruction with little
evidence of mitral regurgitation. The left atrium is mildly enlarged (1.8 cm) with normal auricular emptying velocities. The transmitral flow velocity profile documents E/A reversal consistent with a relaxation abnormality. There is no evidence of pericardial effusion or a cardiac mass lesion. DIAGNOSTIC INTERPRETATION: Today's evaluation is consistent with a diagnosis of hypertrophic obstructive cardio myopathy with moderate hypertrophy and mild left atrial enlargement. There is no evidence of an intra-cavitary thrombus or sontaneous echocardiographic contrast. CLINICAL ASSESSMENT: Today's examination is consistent with a diagnosis of hypertrophic obstructive cardiomyopathy. The degree of hypertrophy coupled with the patient's young age 9 mo. makes me concerned about the long-term prognosis. I believe the severity of the changes places this patient at substantially increased risk for anesthetic complications. I do not recommend general anesthesia unless absolutely necessary. I believe it is reasonable to adopt either an aggressive or conservative appro management would include initiation of the beta blocker (atenolol) at a dose of 1 mg/kg orally twice daily, with gradual up titration to consistently obtain a target heart rate of approximately 130-140 bpm. Additionally, administration of a platelet aggregation inhibitor (clopidogrel or aspirin) could be considered. The mild left atrial enlargement, coupled with the normal auricular emptying velocities suggest that this patient is probably not at markedly increased risk for thromboembolic events however accurate prediction of the risk of these events is challenging. I've placed a call to Dr. Kate Meurs at North Carolina State University to inquire into whether or not she has identified specific genetic mutations in this breed and associated them with early development of hypertrophic cardiomyopathy. Submitting blood to her lab may prove informative. Repeating the echocardiogram in 4-6 months should provide important prognostic information. This reevaluation should be performed whether medical management is started or not.
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Sent from my iPhone using Tapatalk
Michaela L
