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Biomedical subjects

I Kindermann

Publications and source records attributed to I Kindermann.

10 recordsLinked to original sources
PubMed2003

[Detection of left ventricular ischemia at rest by tissue Doppler echocardiography].

UNLABELLED: A 53-year old woman without a previous history of cardiac disease was successfully resuscitated from ventricular fibrillation. Despite a normal two dimensional echocardiogram, tissue Doppler analysis of left ventricular long-axis contraction revealed marked postsystolic contractions in the territory of the left coronary artery suggesting ischemia as the underlying pathogenetic mechanism. This was confirmed by coronary angiography which revealed a high-grade ostial stenosis of the left main stem. After coronary artery bypass surgery, the tissue Doppler findings normalized. CONCLUSION: Assessment of regional long axis function by tissue Doppler echocardiography may yield important additional findings even if two-dimensional echocardiography is apparently normal.

Coronary Angiography↗
PubMed1984

Apolipoprotein E phenotypes and hyperlipidemia.

Apolipoprotein E phenotypes were determined in 361 patients with hyperlipidemia and in controls. The E2 isoform was significantly more frequent in the group of hyperlipidemics (P less than 0.0005). This was not due to a higher frequency of E-2/2 homozygotes with type III hyperlipoproteinemia, but rather to a significantly higher frequency of E2 heterozygotes (P less than 0.0005). Subgrouping of hyperlipidemics into patients with a) hypertriglyceridemia, b) hypercholesterolemia and c) mixed hyperlipidemia revealed i) that isoform E2 was significantly more frequent in patients with hypertriglyceridemia (0.001 greater than P greater than 0.005), ii) that isoform E4 was significantly more frequent in patients with hypercholesterolemia (0.01 greater than P greater than 0.005) and iii) that isoforms E2 (P less than 0.005) and E4 (0.05 greater than P greater than 0.025) were both more frequent in patients with mixed hyperlipidemia. Roughly 20% of patients with mixed hyperlipidemia had one of the rare phenotypes E-4/4, -4/2 or -2/2. We conclude that alleles epsilon 2 and epsilon 4 both contribute to the susceptibility for, and/or phenotypic expression of hyperlipidemia. Whereas the gene epsilon 2 seems to exert its influence on plasma lipoproteins by an abnormal gene product (E2) that has reduced binding activity to lipoprotein receptors, the mechanism underlying the association of the epsilon 4 gene with hyperlipidemia is presently unclear.

Apolipoproteins↗