Hyperhomocysteinemia: an independent risk factor for vascular disease

Article Abstract:

The commonly mentioned risk factors for cardiovascular diseases, namely smoking, high blood pressure and high cholesterol, are not involved in all cases of cardiovascular illness. Genetic susceptibility has probably been underestimated, and its relationship to risk factors has not been clarified. Homocystinuria, a rare biochemical abnormality caused by a metabolic defect during the transformation of the amino acid methionine into cystine, causes mental retardation, skeletal abnormalities and vision problems. Patients with this condition are also at high risk of arteriosclerosis (fatty deposits on artery walls) and blood clots in the veins. This is probably caused by high levels of homocysteine, which is toxic to the lining of the blood vessels, causes oxidation of low-density lipoprotein cholesterol, and promotes clot formation. Although the disease is rare, 1 to 2 percent of the population may have inherited the gene from one parent, and many young patients with vascular disease may have hyperhomocysteinemia. Reports about the role of hyperhomocysteinemia in vascular disease have been contradictory. To clarify the issue, 25 people who had inherited the condition were studied. Twenty-seven normal subjects were used as controls. Results were compared with those obtained from 123 patients who had been diagnosed with vascular disease before the age of 55. Hyperhomocysteinemia was found in 30 percent of patients with premature disease of the blood vessels. The usual prevalence in the general population is two percent for the same age group. The relationship of hyperhomocysteinemia to vascular disease does not seem to be related to other risk factors. Dietary and environmental factors may modify the condition, but it is not clear whether these changes can help reduce vascular disease. (Consumer Summary produced by Reliance Medical Information, Inc.)

Cardiovascular diseases, Physiological aspects, Genetic aspects, Methionine

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The diagnostic performance of computer programs for the interpretation of electrocardiograms

Article Abstract:

It is estimated that 100 million electrocardiogram (ECG) recordings are made each year in the US. Over half of these are interpreted with the help of computer analysis. While there have been a few studies that compared the usefulness of some programs, there has been no comprehensive evaluation of the performance of computer programs in interpreting ECGs. A total of 1,220 electrocardiograms were analyzed, representing 382 control patients and patients with a variety of heart disorders including heart attacks and heart failure. The ECG recordings were analyzed by eight cardiologists and nine computer programs. Both sets of diagnoses based on the ECGs were compared with diagnoses made on the basis of clinical findings independent of the electrocardiographic results. The study revealed that the computer programs fell short of the cardiologists, but not by much. The computer programs correctly identified 91.3 percent of the cases, compared with 96 percent for the cardiologists. The performance of the computer programs varied for different heart problems; the sensitivity of the programs for diagnosing right ventricular hypertrophy was 31.8 percent and 46.6 percent for the cardiologists. Similarly, the sensitivity of the programs for diagnosing myocardial infarction was 77.1 percent and 84.9 percent for the cardiologists. It should be emphasized that there was considerable variation among the computer programs in the analysis of ECG recordings. The best programs nearly matched the performance of the most accurate human cardiologists. (Consumer Summary produced by Reliance Medical Information, Inc.)

Analysis, Evaluation, Medicine, Information management, Computer-aided medical diagnosis, Computer aided medical diagnosis, Electrocardiogram, Electrocardiography

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Coexistence of hereditary homocystinuria and factor V Leiden - effect on thrombosis

Article Abstract:

People with both homocystinuria and factor V Leiden have an increased risk of thrombosis, the formation of blood clots that block blood vessels. Factor V Leiden is a mutated form of factor V that does not respond to activated protein C, an anti-clotting factor. Researchers measured homocysteine levels, partial-thromboplastin times, and analyzed the factor V gene in 45 members of 7 families. Each family had at least one person who had a pair of genes for homocystinuria. Of the 7 people with homocystinuria and factor V Leiden, all but one had thrombosis. The one exception was a baby who had only one factor V Leiden gene and had received anticlotting therapy from birth. Among the 4 people with homocystinuria but no factor V Leiden, none had thrombosis. Three women in one family who had one gene for each homocystinuria and factor V Leiden had spontaneous abortions and circulation disorders in their placentas.

Abnormalities, Complications and side effects, Blood coagulation factors, Thrombosis

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