What is the difference between lvh and hcm

On the other hand, family history of sudden cardiac death in a healthy individual, 10 , is a very rare finding. Thus, in the setting of a borderline cardiac hypertrophy, a positive family history is suggestive of cardiac disease. Still, as a diseased individual may often lack this characteristic, the sensitivity and specificity of such a criterion is low and it would be a weak stand-alone test for the diagnosis of HCM.

Pandian, MD, Barry J. Our mission: To reduce the burden of cardiovascular disease. Help centre. All rights reserved. Did you know that your browser is out of date? To get the best experience using our website we recommend that you upgrade to a newer version. Learn more. Show navigation Hide navigation. Sub menu. References H.

JACC, Klues HG, Schiffers A, Maron BJ: Phenotypic spectrum and patterns of left ventricular hypertrophy in hypertrophic cardiomyopathy: morphologic observations and significance as assessed by two-dimensional echocardiography in patients. Circulation ; N Engl J Med ; B. Ethnic differences in left ventricular remodeling in highly-trained athletes relevance to differentiating physiologic left ventricular hypertrophy from hypertrophic cardiomyopathy.

Secondary obstruction of the left ventricular outflow tract LVOT may worsen LV hypertrophy through additional pressure overload. Furthermore SAM may be observed in very young or quite old cats without any LVH, when echocardiography is performed to detect the source of a new murmur.

A similar albeit rare phenomenon has been described in dogs by D'Agnolo and others. The question arises concerning the development and the classification of this entity; experimentally, SAM can be produced by displacement of the anterior papillary muscle. Possibly, the cause of 'primary SAM' is different in young, and in older cats.

In young cats a congenital abnormality of the anterior papillary muscle resulting in an abnormal attachment of the chordae tendineae and mitral valve may be the cause; this entity probably should be classified as mitral valve dysplasia. In older cats with a new heart murmur and 'primary SAM', myocardial and especially papillary muscle remodelling secondary to inflammatory, toxic or ischaemic insults may responsible. These entities should rather be classified as secondary cardiomyopathies.

Myocarditis has been known for many years to cause abnormal myocardial function and cardiac dilation in humans. Many cases of dilated cardiomyopathy DCM are actually caused by myocarditis. In humans, myocarditis is therefore classified as primary mixed cardiomyopathy. Myocarditis in cats is also well recognised. The authors have examined several cats that had developed pulmonary oedema associated with anaesthesia or surgery, and that on echocardiography had shown LVH and left atrial dilation typical of HCM.

Supportive therapy including diuretics and oxygen led to resolution of the congestion and clinical normalisation. Repeated echocardiography showed a successive regression of LVH and left atrial dilation.

This presentation and disease course argue against primary HCM, but rather for a reversible damage such as infectious or toxic myocarditis. A similar picture, as in the suspected myocarditis cases with acute congestive heart failure, has been reported in cats after the administration of steroids. Such cats, initially diagnosed with HCM due to LV hypertrophy and left atrial dilation not only recovered clinically from congestive heart failure but also normalised echocardiographically.

Nevertheless, attempts to elicit this form of cardiomyopathy experimentally were unsuccessful. The question arises whether a genetic predisposition is required to react in this fashion to steroids, or alternatively if affected cats in fact had myocarditis associated with glucocorticoid administration. Thyroid hormones have important metabolic and cardiovascular effects. Hyperthyroidism causes an increased metabolic rate which demands an increased cardiac output.

In the periphery thyroid hormones cause a decreased vascular resistance. In the myocardium, thyroid hormones induce multiple genes causing LV hypertrophy. After recruiting patients, collecting the baseline data, a CMR scan will be carried out and post-processed, a predetermined differentiating formula including left ventricular morphology, ejection fraction, presence of late gadolinium enhancement, T1 value and strain data will be used to produce a cardiac values, which is to be input into our differentiating flow.

The diagnosis of hypertensive heart disease was based on medical history and conventional echocardiography. The healthy age-matched controls were generally volunteers with a normal electrocardiogram, normal echocardiographic examination, and overall normal CMR findings. Outcome Measures. Primary Outcome Measures : validation of the algorithm in all patients [ Time Frame: after post-procession and complete the flow chart within 24 hours ] Evaluate the area under the curve of our algorithm compared with single parameter wall thickness, strain in all patients.

Eligibility Criteria. Information from the National Library of Medicine Choosing to participate in a study is an important personal decision. Consecutive subjects were prospectively enrolled into 3 cohorts between July and June The cohorts were divided as follows: the hypertrophic cardiomyopathy, hypertensive heart disease and control groups.

Contacts and Locations. Information from the National Library of Medicine To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor. Please refer to this study by its ClinicalTrials.

More Information. National Library of Medicine U. National Institutes of Health U. Department of Health and Human Services. The safety and scientific validity of this study is the responsibility of the study sponsor and investigators.