Introduction: The high morbidity and mortality by hypertensive cardiopathy demand the construction and validation of tools to stratify the risk of developing this condition.
Objective: To design and validate an index, based on risk factors, that permits to predict the development of hypertensive cardiopathy in patients with a diagnosis of essential arterial hypertension.
Methods: A prospective cohort study was done in hypertensive patients assisted at the specialized arterial hypertension physicians’ office of the “Carlos Manuel de Céspedes” Specialty Policlinic attached to the General University Hospital, Bayamo Municipality, Granma Province, Cuba from January 1st, 2010 to December 31, 2016. Internal and external validity and the internal consistency of the index were determined.
Results: The index sensitivity was of 97, 20 (IC: 93, 93-94.09) and specificity of 65, 38 (IC: 76, 25-76, 20). Both the index discriminative capacity (area under the ROC curve= 0,944; interval of confidence: 0.932-0.956; p<0.0005) and calibration (p=0.751) were adequate.
Conclusions: The present study proposes an index to predict the risk of developing hypertensive cardiopathy, with adequate discriminative capacity and calibration (external validity). The index can be used as a tool of clinical and epidemiological surveillance since it permits to identify subjects with greater probability of developing the condition and to stratify the risk.
Founder mutations are rare causes in arrhythmogenic cardiomyopathy including TMEM43 und phospholamban mutations. The incidence is approximately 1%. P.S358L TMEM43 mutations cause aggressive, in most cases biventricular arrhythmogenic cardiomyopathy , with the necessity of primary prophylactic ICD implantation in men and in women>30 years for sudden cardiac death prevention.The mutation increases the stiffness of the cell nucleus thus producing the massive loss of cardiomyocytes . P.Arg14del phospholamban mutations cause biventricular arrhythmogenic cardiomyopathy with predominant heart failure, and in some cases, secondary sudden cardiac death . Both founder mutations have characteristic electrocardiographic appearance, together with typical ECG manifestations of arrhythmogenic cardiomyopathy like right precordial T-wave inversions, terminal activation delay and epsilon waves in right precordial leads. Typical ECG manifestations in TMEM43 mutations are poor R-wave progression in right precordial leads (Figure 1), often associated with T-wave inversions in lateral leads . Typical ECG manifestations in phospholamban mutations are low voltage ECG , more than complete right bundle branch block , epsilon waves in right precordial leads and in lead aVR  and right precordial T-wave inversions (Figure 2). Atrial fibrillation occurs frequently.
In order to suggest new pathogenetic hypotesys in some heart disease we think is interesting to observe some biomedical literature: Can we think some endogenus toxicologic movens in some heart pathologies?
Activated platelet can trigger coronay artery spasm in some patients, and in SCD many patients not show Anatomic abnormalities and this can be involved sudden vigorous exertion untrained subjects (also in young) in seems to show an inadeguate methabolic response. Also severe artmia can be due by electrolyte umbalance.
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