Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of propranolol and diltiazem on left ventricular systolic and diastolic function in hypertensive subjects (DBP 90-114 mmHg) were examined with M-mode and 2D echocardiograms in 21 patients in a double-blind fashion prior to and after 4 months of treatment. Systolic function was assessed by measurement of fractional shortening, mean velocity of fibre shortening, peak systolic pressure/end systolic dimension ratio, and end systolic stress/end systolic dimension ratio. To assess diastolic function, maximal rate of change in left ventricular dimension (MAXD), maximal rate of change in posterior wall thinning (MAX PWT) and early diastolic (EDD) and late diastolic dimension changes (LDD) were calculated using digitised M-mode images of mid-wall diameter. Both propranolol and diltiazem reduced systolic and diastolic pressures similarly. No significant changes were observed in any of the parameters of systolic function with either drug. Similarly neither propranolol nor diltiazem altered MAXD or EDD significantly. Although changes in maximal rate of posterior wall thinning (MAX PWT) were not significant with either drug, diltiazem improved MAX PWT in 7 of 8 patients. The results of the study demonstrate that both propranolol and diltiazem reduce blood pressure without significant deleterious effects on systolic or diastolic function. Diastolic functional parameters, which were not abnormal at baseline, showed no consistent change with either propranolol or diltiazem.
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PMID:Comparative effects of propranolol and diltiazem on systolic and diastolic left ventricular function in essential hypertension. 209 10

To assess the time-course of adaptive responses of the left ventricle to chronic volume overload, dogs were instrumented with a left ventricular (LV) micromanometer and pairs of ultrasonic crystals for the measurement of LV wall thickness (WTh), LV chamber diameter (D), and longitudinal segment length (L). Following a control study, mitral regurgitation (MR) was created by a transventricular section of the chordae tendineae. Heart rate was controlled during each study by atrial pacing. Plasma norepinephrine levels at rest were determined by high-performance liquid chromatography. Eight days (mean) after the onset of MR, enddiastolic (ED) D had increased by 9% from 34.2 +/- 2.4 mm (SEM) (P less than 0.001), with significant thinning of the wall thickness (from 8.2 to 7.7 mm, P less than 0.001). Consequently the calculated cross-sectional area (CSA) of the left ventricular wall remained the same. Peak wall stress (WSt) and EDWSt increased by 20% and 152%, respectively. During the subsequent 4 weeks, EDD progressively increased, averaging 11% above the control at 4 weeks, while EDWTh returned to the control level. Thus, the development of hypertrophy was clearly evidenced by an increase in CSA (by 8% over the control, P less than 0.001). These changes were accompanied by a consistent reduction in both peak WSt and EDWSt. Mean velocity of circumferential fiber shortening (meanVcf) and percentage shortening were significantly augmented following the onset of MR and remained at the same level thereafter, indicating no further use of the Frank-Starling mechanisms during chronic ventricular dilation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adaptations of the left ventricle to chronic volume overload induced by mitral regurgitation in conscious dogs. 293 15