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Biomedical subjects

H C Mehmel

Publications and source records attributed to H C Mehmel.

At least 55 records · Page 3Linked to original sources
PubMed1981

[Effect of intracoronary fibrinolysis on left ventricular diastolic function in patients with acute myocardial infarction (author's transl)].

In 22 patients with acute myocardial infarction, intracoronary infusion of streptokinase was begun 3.2 +/- 1.4 hours after the onset of symptoms. In 71% of patients recanalization of a completely occluded artery could be achieved. In 12 successfully treated patients left ventricular hemodynamics (left ventricular diastolic compliance and regional wall motion) were compared before and 4 weeks after recanalization. 4 weeks after intracoronary fibrinolysis left ventricular end-diastolic pressure had fallen (from 20 to 15 mm Hg, p less than 0.05), diastolic compliance had improved (p less than 0.05) and infarct size was reduced (p less than 0.05) compared to the acute stage of myocardial infarction. Left ventricular hemodynamics of 16 patients without heart disease (group A) and 22 patients with chronic myocardial infarction treated medically (group B) were compared to the findings of patients with acute myocardial infarction (group C). Group B and C showed reduced diastolic compliance as compared to group A (p less than 0.001). When group B and c were compared with identical size of akinesis (as measured by the number of asynergic hemiaxes), there was no significant difference of diastolic compliance. Reduction of diastolic compliance correlated linearly with infarct size (r = 0.73, r = 0.78). The results indicate that successful early reperfusion of acute myocardial infarction leads to a reduction of infarct size.

Adult↗
PubMed1979

[Coronary reserve, left ventricular function, and coronary risk factors in patients with myocardial infarction, but normal coronary arteries (author's transl)].

In 5 patients with angiographically normal coronary arteries and previous myocardial infarction (left ventricular a- or dyscinesia), measurement of coronary reserve revealed normal values. On average, patients with myocardial infarction and normal coronary arteries were younger than patients with angiographically proven obstructive coronary lesions (p less than 0,001), and did not exhibit a rise in coronary risk factors. These results suggest that in some cases myocardial infarction is due to acute, completely reversible occlusion or severe stenosis of larger coronary arteries without morphological or functional defects of coronary arteries detectable later on.

Adult↗
PubMed1977

[Functional assessment of coronary-artery stenosis (author's transl)].

Left-ventricular angiography was performed in 28 patients after measuring ascending aortic and left ventricular pressures and during isometric exercise (hand grip, 0.3-0.4 kg/cm2 for 3 min). In 13 patients coronary blood flow was measured at rest and during hand-grip exercise by means of the argon method. Eight patients without heart disease served as controls. In 14 patients with coronary heart disease abnormal left-ventricular kinetics, demonstrated already at rest, got worse during hand-grip exercise. In five patients with normal left-ventricular angiograms at rest hypokinesia and dyskinesia occurred during isometric exercise. The coronary artery supplying the abnormal ventricular wall had a 50-75% decrease in diameter. One patients with isolated 25% stenosis had normal left-ventricular kinetics both at rest and on hand-grip exercise. In all patients coronary blood flow rose by 60-90% during isometric exercise. It iducing a significant rise in myocardial oxygen demand and increased coronary blood flow.

Angiography↗
PubMed1976

The influence of hypertrophy on myocardial function.

In patients with hypertrophy from long-standing left ventricle pressure (PL) and volume overload (VL) as well as in a group of controls basal left ventricular contractility was assessed by peak measured isovolumic velocity of shortening (Vpm), mean velocity of circumferential fiber shortening (mean VCF) and mean normalized systolic ejection rate (MNSER). The angiographically determined left ventricular muscle mass was elevated to a similar extent in PL and VL. As compared to the control group both hypertrophy had decreased contractile indexes. No significant differences of contractility existed between the groups with PL and VL. Hence it appears that in chronic mechanical overloading the extent of hypertrophy is probably more important for the decrease of contractility than the nature of the stimulis to hypertrophy. In 15 patients with aortic stenosis left ventricular muscle mass and isovolumic and ejection phase contractile indexes were determined preoperatively and 13.5 months after successful valve replacement by a tilting disc prosthesis. Postoperatively there was a significant (P less than 0.001) decrease of muscle mass from 182 to 114 g/m2. Mean VCF increased from 1.07 to 1.52 circ/sec (P less than 0.01); MNSER from 1.92 to 2.59 enddiastolic volumes/sec (P less than 0.01); Vpm from 1.17 to 1.60 ML/sec (P less than 0.001) and total pressure Vmax from 1.61 to 2.09 ML/sec (P less than 0.01). In 9 of 13 patients an abnormal or pathologic response to handgrip at the preoperative study became normal postoperatively. It is concluded that in aortic stenosis removal of the chronic pressure burden leads to regression of left ventricular hypertrophy associated with an improvement of resting and exercise contractile function. Pressure-deprived contractile indexes; ejection phase contractile indexes; chronic pressure load; chronic volume load; aortic valve replacement; postoperative hemodynamics.

Cardiomyopathy, Hypertrophic↗
PubMed1975

Contractility of the hypertrophied human left ventricle in chronic pressure and volume overload.

Nine patients with normal left ventricles (C), 10 patients with pressure load (PL) due to predominant aortic stenosis, and 9 patients with predominant volume load (VL) due to aortic incompetence were studied by left ventricular high-fidelity pressure measurements and cineangiography. Peak measured velocity of the contractile elements (Vpm) used as index of contractility and left ventricular muscle mass (LMMI) were determined. The patients with PL and VL were matched with respect to LMMI. In PL LMMI was 241 +/- 41 and in VL 254 +/- 42 gm. per square meter. Both were sizably increased (P smaller than 0.001) as compared to LMMI in C (89 +/- 24 gm. per square meter). Vpm was 1.41 +/- 0.20 ML per second in C. In PL and VLVpm was reduced to 1.05 +/- 0.26 (P smaller than 0.01) and to 1.07 +/- 0.33 ML per second (P smaller than 0.02). Vpm in PL was not different from Vpm in VL. Heart rate showed no major difference in the three groups. It is concluded that in two groups of patients with predominant PL and VL matched with respect to LMMI left ventricular contractility was depressed to a similar extent regardless of the stimulus to hypertrophy.

Animals↗