Biomedical subjects

O M Hess

Publications and source records attributed to O M Hess.

At least 127 records · Page 7Linked to original sources

PubMed1993

Influence of serum cholesterol and other coronary risk factors on vasomotion of angiographically normal coronary arteries.

BACKGROUND: It has been shown that there is impairment of the vasodilatory response to acetylcholine in patients with hypercholesterolemia and angiographically normal coronary arteries. Moreover, in patients with angiographically smooth coronary arteries, the number of coronary risk factors is associated with a loss of endothelium-dependent vasodilation. The purpose of the present analysis was to evaluate in patients with and without coronary artery disease coronary vasomotor response to dynamic exercise in angiographically normal and stenosed coronary arteries and to relate the response to serum cholesterol levels as well as to other coronary risk factors. METHODS AND RESULTS: Luminal area change during exercise (delta-ex, percent change compared with rest = 100%) was determined by biplane quantitative coronary arteriography in three groups: Group 1 consisted of 14 patients with normal total serum cholesterol of < 200 mg/100 mL; mean, 173 mg/100 mL (mean age, 51 years). Group 2 comprised 23 patients with a slightly elevated cholesterol of 200 to 250 mg/100 mL; mean, 223 mg/100 mL (mean age, 53 years). Group 3 had 24 patients with markedly elevated cholesterol of > 250 mg/100 mL; mean, 288 mg/100 mL (mean age, 54 years). Serum cholesterol levels and categorical risk factors such as positive family history, history of hypertension, smoking, obesity, and diabetes were related to exercise-induced vasomotor response. The three groups did not differ with regard to clinical characteristics, exercise work load, and hemodynamic data measured during exercise. However, delta-ex in normal vessels was significantly different between all three groups (ANOVA, P < .01): +31% (group 1), +18% (group 2), and +4% (group 3). Delta-ex in stenotic vessels did not differ between the groups: -5% (group 1), -13% (group 2), and -12% (group 3). Delta-ex of the nonstenosed vessel correlated significantly and inversely with total cholesterol, with low-density lipoprotein cholesterol, with the ratio of total to high-density lipoprotein cholesterol, and with the number of coronary risk factors present in a patient. High total cholesterol and a history of hypertension were independent risk factors for impaired coronary vasomotion. CONCLUSIONS: In patients with and without coronary artery disease, hypercholesterolemia and a history of hypertension independently impair exercise-induced coronary vasodilation in angiographically normal coronary arteries. In the stenotic vessel, vasomotion during exercise does not appear to be influenced by the actual serum cholesterol. The precise mechanism by which the impaired vasomotion of the angiographically normal coronary arteries is mediated is unknown, but a direct negative effect of hypercholesterolemia on endothelial function or early undetected atherosclerosis appears to be the most likely explanation.

Cholesterol↗

PubMed1993

Regional left ventricular mechanics in hypertrophic cardiomyopathy.

BACKGROUND: Nonuniformity is a determinant of diastolic function. In patients with hypertrophic cardiomyopathy, hypertrophy, abnormal calcium handling, and regional ischemia can also play a role. This study was designed to assess regional mechanics, asynchrony, and asynergy in patients with hypertrophic cardiomyopathy. METHODS AND RESULTS: Nine control subjects and 22 patients with hypertrophic cardiomyopathy were studied by biplane left ventriculography and high-fidelity pressure tracings for the assessment of diastolic function by computing the time constant of isovolumic relaxation, peak filling rate, and the constant of passive chamber stiffness. Regional mechanics were evaluated by dividing the left ventricle into six sectors in the right and left anterior oblique projections. Systolic and diastolic asynchrony were assessed from the coefficient of variation of the regional time intervals from end diastole to end systole and to peak filling rate, respectively. Asynergy was evaluated from the coefficient of variation of the regional area reduction. Regional passive elastic properties were estimated by computing the regional constant of chamber stiffness. In patients with hypertrophic cardiomyopathy, isovolumic relaxation was prolonged (time constant of isovolumic relaxation 101 +/- 41 versus 51 +/- 16 milliseconds in control subjects; P < .001) and the constant of chamber stiffness was increased (0.056 +/- 0.038 versus 0.025 +/- 0.010 mL-1; P < .001). Both systolic and diastolic asynchrony as well as asynergy were found. Regional mechanics showed hyperkinesia in the free wall, whereas the septum exhibited normal wall motion and increased constant of chamber stiffness. CONCLUSIONS: Diastolic function is impaired in hypertrophic cardiomyopathy, and such an impairment is the consequence of nonuniformity and hypertrophy. The regions where the myopathic process is more pronounced show normal wall motion but increased stiffness. The inhomogeneity of regional wall motion with regional hyperkinesia and normokinesia of neighboring regions results in left ventricular asynergy.

Adult↗

PubMed1993

[Hemodynamics in heart failure: systolic and diastolic dysfunction].

Cardiac insufficiency is hemodynamically characterised by reduced cardiac output and increased diastolic filling pressure at rest and/or during physical activity. The increase in diastolic filling pressure compensates cardiac output and is either a result of increased initial tension of muscle fibers (Frank-Starling's Law) or a sign of decreased myocardial compliance. Increased initial tension of muscle fibers is a sign of systolic insufficiency, whereas reduced ventricular compliance indicates a disorder of diastolic ventricular function. In systolic insufficiency (= systolic dysfunction) a decrease in the ventricular ejection fraction is important, as is an increase in filling pressure. In diastolic congestive heart failure (= diastolic dysfunction) a reduced ventricular compliance with normal stroke function is typical.

Diastole↗

PubMed1993

Diastolic dysfunction in aortic stenosis.

Diastolic dysfunction is characterized by an increased resistance to filling with increased diastolic filling pressures. A variety of disorders are associated with diastolic dysfunction, such as hypertrophy, structural alterations of the myocardium with increased fibrosis, myocardial scarring, or infiltrative processes. In addition to these changes, physiological abnormalities of the left ventricle with impaired relaxation, decreased diastolic filling, and increased stiffness of the myocardium can be observed. In patients with aortic stenosis, the most common cause for diastolic dysfunction is left ventricular hypertrophy. Diastolic dysfunction is found in approximately 50% of the patients with normal systolic ejection performance and in 100% of the patients with depressed function. Diastolic function appears either to be more sensitive for detection of abnormal left ventricular function in patients with aortic stenosis or to precede systolic dysfunction or both. Treatment of diastolic dysfunction is usually achieved by aortic valve replacement with regression of left ventricular hypertrophy, but in patients with decompensated aortic stenosis, a reduction of circulating blood volume to reduce diastolic filling pressures, and thus dyspnea, is often indicated. Prognosis of patients with diastolic dysfunction is usually better than that of patients with systolic dysfunction but is clearly worse than that of normal patients.

Aortic Valve Stenosis↗

PubMed1992

Effect of progression of left ventricular hypertrophy on coronary artery dimensions in aortic valve disease.

OBJECTIVES: The effect of progression of left ventricular hypertrophy on coronary artery dimensions was studied in patients with aortic valve disease. METHODS: Cross-sectional area of the left and right coronary arteries was determined by quantitative coronary arteriography in 12 control subjects and in 10 patients with aortic valve disease at baseline and after a follow-up period of 66 months. RESULTS: The cross-sectional area of the left coronary artery was larger in patients with aortic valve disease than in control subjects (left anterior descending artery 13 vs. 8 mm2, p < 0.001; left circumflex artery 13 vs. 6 mm2, p < 0.001). At the follow-up examination, cross-sectional area of the left coronary artery increased (left anterior descending artery 17 mm2, p < 0.01 vs. baseline; left circumflex artery 15 mm2, p < 0.01 vs. baseline). The cross-sectional area of the right coronary artery was not different in patients with aortic valve disease from that in control subjects. Left ventricular muscle mass was larger in patients with aortic valve disease both at baseline (269 g, p < 0.001) and after follow-up examination (339 g, p < 0.001) than in control subjects (136 g). The appropriateness of coronary artery size with respect to muscle mass was evaluated by normalizing cross-sectional area of the left coronary artery (left anterior descending plus left circumflex artery) per 100 g of left ventricular muscle mass (mm2/100 g). This index was 10.9 mm2/100 g in control subjects, and decreased in subjects with aortic valve disease from 10.3 mm2/100 g at baseline to 8.6 mm2/100 g at the follow-up measurement (p < 0.05 vs. control values). CONCLUSIONS: In patients with aortic valve disease, the progression of left ventricular hypertrophy is associated with an increase in left anterior descending and left circumflex coronary artery dimensions, whereas the size of the right coronary artery remains unchanged. Despite the enlargement of the left coronary artery, the cross-sectional area of the left coronary artery per 100 g of left ventricular muscle mass decreased. Hence, the increase in coronary artery size appears to be inadequate when the severity of left ventricular hypertrophy increases.

Adult↗

PubMed1992

Decreased concentration of myofibrils and myofiber hypertrophy are structural determinants of impaired left ventricular function in patients with chronic heart diseases: a multiple logistic regression analysis.

OBJECTIVES: The aim of this study was to perform a multiple logistic regression analysis to identify independent structural determinants of impaired left ventricular function. BACKGROUND: The association between contractile failure and structural alterations of the myocardium has been demonstrated in several studies, and multiple interactions between myocardial structure and cardiac performance are likely. METHODS: Morphometric data assessed from 130 left ventricular biopsy specimens were analyzed. The endomyocardial specimens were obtained from 57 patients with normal coronary arteries (17 with normal left ventricular ejection fraction and 40 with impaired left ventricular function [dilated cardiomyopathy]), 15 patients with hypertrophic cardiomyopathy and 32 patients with aortic valve disease. Transmural biopsy specimens were assessed in 6 donor hearts before heart transplantation and in 20 patients with left anterior descending coronary artery disease whose specimens were obtained from the left ventricular anterior wall during aortocoronary bypass surgery. Global or regional left ventricular function was evaluated from left cineventriculograms. The volume fraction of cardiac fibrous tissue, intracellular volume fraction of myofibrils, volume fraction of myofibrils related to myocardial tissue (including fibrosis) and myofiber diameters were determined from semithin sections of the biopsy specimens with the use of light microscopic morphometry. RESULTS: Multiple logistic regression analysis revealed decreased volume fraction of myofibrils (p < 0.005) and increased fiber diameter (p < 0.002) as independent determinants of impaired left ventricular function. CONCLUSIONS: These data indicate that, independent of the underlying heart disease, both decreased concentration of contractile proteins and myocyte hypertrophy are independently associated with impaired left ventricular function.

Age Factors↗

PubMed1992

[Digital subtraction angiography for the assessment of myocardial perfusion].

Coronary angiography does not only permit to evaluate the severity of coronary disease but also to assess coronary flow reserve in various myocardial perfusion areas by digital processing. Use of colour flow mapping allows the assessment of both, density as well as distribution velocity of contrast-medium (= parametric imaging). The advantage of this technique is given by the possibility to assess coronary flow reserve not only at rest but also under physiologic situations such as bicycle ergometry. Clinical investigations have shown that coronary flow reserve determined after papaverine administration does not correlate with physiologic conditions such as physical exercise.

Angiography, Digital Subtraction↗

PubMed1992

Effect of aortic valve stenosis (pressure overload) and regurgitation (volume overload) on left ventricular systolic and diastolic function.

In secondary hypertrophy from chronic pressure or volume overload, or both, systolic as well as diastolic abnormalities of left ventricular (LV) function have been described, but their relation has not been defined. In 58 patients with aortic valve disease (28 with aortic valve stenosis, and 30 with aortic regurgitation) and in 11 control subjects, LV biplane cineangiography was performed simultaneously with LV high-fidelity pressure measurements. LV ejection performance was assessed by ejection fraction, and diastolic function by the time constant of LV pressure decay, the early and late peak filling rates, and the constants of chamber (pressure-volume relation) and myocardial stiffness (stress-strain relation). In the entire cohort (n = 69), ejection fraction was inversely related to the time constant of LV relaxation (r = -0.58, p less than 0.001) and to the constant of myocardial stiffness (r = -0.62, p less than 0.001). Despite preserved systolic contractile function (as evaluated from the ejection fraction-mean systolic stress relation), abnormalities in LV diastolic function were present in 9 of 18 patients with pressure overload and 20 of 22 with volume overload. None of the 58 patients with aortic valve disease had a reduced early peak filling rate, whereas a reduction in late peak filling rate was observed in 3 with aortic stenosis, but in none with aortic regurgitation. This, it appears that abnormalities of relaxation and passive diastolic myocardial stiffness precede alterations in myocardial contractility. Assessment of peak filling rates is not helpful to detect diastolic dysfunction in patients with aortic valve disease.

Adolescent↗

PubMed1992

Coronary tandem lesions: effect of exercise.

Coronary vasomotion of two stenoses in series (i.e., tandem lesion) was studied in 10 patients with coronary artery disease. Percent area stenosis was 69% +/- 23% for the first (S1) lesion and 70% +/- 37% for the second (S2). Quantitative coronary arteriography was carried out at rest, during two levels of exercise (2 minutes, 75 W and 1.9 minutes, 100 W), and at 5 minutes after sublingual administration of 1.6 mg nitroglycerin. Both stenoses showed exercise-induced vasoconstriction (S1: -29%, p less than 0.01 versus rest; S2: -29%, p less than 0.01 versus rest), which was reversible after sublingual administration of nitroglycerin (S1: +15%, not significant versus rest; S2: +13%, not significant versus rest). The vessel segment between the two stenoses showed no vasomotion during exercise, whereas the pre- and poststenotic "normal" vessel segment elicited exercise-induced vasodilation. There was an inverse relationship between percent area stenosis of the second lesion and exercise-induced vasoconstriction of the first lesion (correlation coefficient = 0.84). The more severe the distal stenosis was, the less exercise-induced stenosis narrowing of the proximal lesion was observed. Thus it is concluded that coronary vasomotion of two stenoses in series is dependent on both active and passive mechanisms because both lesions show exercise-induced vasoconstriction, but vasomotion of the proximal lesion is dependent on the severity of the second one.

Adult↗

PubMed1992

Cutaneous and coronary flow reserve in patients with microvascular angina.

Microvascular angina is characterized by exercise-induced angina in patients with normal coronary arteries and reduced coronary flow reserve. Recently, a generalized disorder of abnormal vascular reactivity in microvascular angina has been postulated. Therefore, coronary flow reserve was determined by the coronary sinus thermodilution technique and compared with the cutaneous flux ratio in 6 control subjects (group 1) and 12 patients with microvascular angina (group 2). Coronary flow reserve was calculated from maximal coronary flow after 0.5 mg/kg of dipyridamole divided by flow at rest. Cutaneous flow ratio was estimated by laser Doppler fluxmetry (right forearm) before and after 4 min of suprasystolic blood pressure occlusion. Coronary flow at rest was identical in the two groups, but after maximal vasodilation with dipyridamole, coronary flow was higher in group 1 than in group 2 (p less than 0.05). Coronary flow reserve differed significantly between the two groups (2.9 in group 1 and 1.3 in group 2; p less than 0.001). Cutaneous Doppler flux at rest was higher in group 1 than in group 2 (p less than 0.05). However, the hyperemic response was identical in both groups. It is concluded that the cutaneous flux ratio in patients with microvascular angina is not impaired. Local peripheral vasomotor tone appears to be increased in patients with microvascular angina because cutaneous flow at rest is reduced. Thus, a generalized disorder of abnormal vascular reactivity cannot be confirmed in patients with microvascular angina.

Adult↗

PubMed1992

Fluorescence spectroscopy for identification of atherosclerotic tissue.

OBJECTIVE: Vessel perforation and limited steerability of the laser light are the major limitations of laser angioplasty. To improve steerability fluorescence spectroscopy has been proposed for identification of atherosclerotic plaques. The aim was to investigate this. METHODS: Fluorescence spectroscopy with three different excitation wavelengths (325 nm, 380 nm, 450 nm) was tested in an emission range of 400 nm to 600 nm. Intensity ratios at 480/420 nm were determined in different types of blood vessels. Necropsy material from 40 patients (punch biopsies of 4 mm diameter from the coronary and carotid artery as well as from the ascending and descending aorta) was studied spectroscopically. Histological alterations of the vessel wall were assessed by a semiquantitative score (0 to 10 points): (a) normal tissue, 0 to 2 points (mean = 0.25; n = 38); (b) mild atherosclerotic lesions, 3 to 5 points (mean = 3.35; n = 39); (c) severe atherosclerotic lesions, greater than or equal to 6 points (mean = 6.75; n = 43). RESULTS: Best spectroscopic results were obtained with an excitation wavelength of 325 nm. In samples with severe atherosclerotic lesions the fluorescence spectra showed a significant reduction of the emitted wavelength intensities when compared to normal tissue. There was a clear separation of the fluorescence spectra between normal and mild as well as between normal and severe atherosclerotic lesions; normal tissue showed an increased intensity in the range from 420 nm to 540 nm, whereas atherosclerotic lesions had no or only a small peak at 480 nm. There was a significant correlation between the semiquantitative score (n = 120) and the fluorescence ratio at 480/420 nm (excitation wavelength 325 nm) with a correlation coefficient of 0.87. The spectroscopic results showed no differences between the samples taken from different types of vessels. CONCLUSIONS: Fluorescence spectroscopy allows a reliable identification of normal and atherosclerotic lesions. The close correlation between the emitted light intensity ratio at 480/420 nm and the histological alterations of the vessel wall suggests a relationship between vessel wall fluorescence and the atherosclerotic alterations of the wall.

Adolescent↗

PubMed1992

Preservation of myocardial function by mechanical circulatory support during prolonged ischaemia.

The effect of mechanical circulatory support on left ventricular (LV) function was evaluated during prolonged myocardial ischaemia. Regional wall thickening of a normal and an ischaemic LV region were determined in eight calves (mean body weight 76 kg) using pairs of ultrasonic crystals. LV end-diastolic (mmHg) and peak systolic (mmHg) pressure as well as maximum dP/dt (mmHg s-1) were calculated from LV high-fidelity pressure tracings. The left circumflex coronary artery was ligated proximally for 6 h and reperfused for 18 h. Circulatory support by the assist device was performed from the beginning of ischaemia to the end of the experiment. After a mean time of 4 h all animals showed ventricular fibrillation, which was converted successfully in six animals after a mean time interval of 5 h. Five animals survived after 24 h. The non-surviving animals had larger infarcts, greater creatine kinase release and a larger drop in cardiac output during ischaemia. Haemodynamic measurements were carried out after turning off the assist device. Inotropic stimulation with 0.68 mg.min-1 dopamine i.v. was performed at the end of the study. LV regional function showed systolic bulging during myocardial ischaemia. After 18 h of reperfusion, the ischaemic wall recovered and showed normal systolic wall thickening in the presence of an increased LV preload. LV relaxation was prolonged after reperfusion, suggesting diastolic dysfunction. It is concluded that mechanical circulatory support is effective in protecting myocardial function during prolonged ischaemia in approximately two-thirds of the animals, despite severe ischaemic ventricular dysfunction and intermittent ventricular fibrillation.

Animals↗

PubMed1992

Normalization of coronary vasomotion after percutaneous transluminal coronary angioplasty?

BACKGROUND: Coronary vasomotion was evaluated at rest and during bicycle exercise in 33 patients (age, 53 +/- 7 years) with coronary artery disease. In a first group of patients (n = 15), vasomotion was studied before and 4.3 +/- 2.3 months (early) after percutaneous transluminal coronary angioplasty (PTCA), whereas in a second group (n = 18), exercise coronary arteriography was performed 30 +/- 11 months (late) after successful PTCA. Patients with restenosis (percent area stenosis greater than or equal to 75% or percent diameter stenosis greater than or equal to 50%) were excluded. METHODS AND RESULTS: Luminal areas of a normal segment and the stenotic segment were determined at rest, during supine bicycle exercise, and 5 minutes after sublingual nitrate administration by using biplane quantitative coronary arteriography. Work loads before and early after PTCA were identical in group 1 and similar late after PTCA in group 2. Percent area stenosis decreased from 86% to 36% (p less than 0.001) in group 1 and from 93% to 46% (p less than 0.001) in group 2. Normal coronary arteries showed mild vasodilation during exercise before (+3%, NS versus rest), early (+7%, NS versus rest), and late after (+10%, p less than 0.05 versus rest) PTCA. Administration of sublingual nitrate was associated with significant vasodilation of the normal vessel segment before (+27%, p less than 0.001 versus rest), early (+31%, p less than 0.001 versus rest), and late (+21%, p less than 0.001 versus rest) after PTCA. In contrast, the stenotic vessel segments showed coronary vasoconstriction during exercise before PTCA (-25%, p less than 0.001 versus rest), whereas minimal vasomotion was observed early (+2%; NS versus rest) as well as late (+5%; NS versus rest) after PTCA. Individual post-PTCA (early and late) exercise data elicited vasodilation in 19, no vasomotion in four, and vasoconstriction in 10 instances. Sublingual administration of nitrate was associated with a significant increase in minimal luminal area before (+18%, p less than 0.05 versus rest), early (+24%, p less than 0.01 versus rest), and late (+16%, p less than 0.001 versus rest) after PTCA. An inverse linear correlation was found between the percent change in minimal luminal area during peak exercise and percent area stenosis at rest (r = 0.77, p less than 0.001). CONCLUSIONS: Exercise-induced stenosis narrowing is observed before PTCA but normal vasomotion is reestablished in two thirds of all patients early and late after PTCA. In one third, an abnormal reaction to exercise (i.e., vasoconstriction) persisted after PTCA, mainly in those patients with a residual area stenosis of 50% (percent diameter stenosis of 30%) or more. Thus, PTCA appears to have a salutary effect on coronary vasomotion during exercise, which, however, remains dependent on the severity of the residual stenosis.

Adult↗

PubMed1992

Regression of coronary artery dimensions after successful aortic valve replacement.

BACKGROUND: The effect of regression of myocardial hypertrophy on coronary artery dimensions was evaluated in patients with aortic valve disease who underwent valve replacement. METHODS AND RESULTS: Cross-sectional area (CSA) of the three major coronary arteries (left anterior descending [LAD], left circumflex [LCx], and right coronary artery) was determined by quantitative coronary arteriography in 15 patients with aortic valve disease before and 38 months (range, 14-113 months) after successful aortic valve replacement. Twelve normal subjects served as controls. Left ventricular (LV) angiographic mass was calculated according to the method of Rackley. CSA of the left coronary artery was larger in aortic valve disease than in controls (LAD, 15 versus 8 mm2, p less than 0.001; LCx, 14 versus 6 mm2, p less than 0.001). After valve replacement, CSA of the left coronary artery decreased (LAD, 12 mm2, p less than 0.05 versus before surgery; LCx, 11 mm2, p less than 0.05 versus before surgery) but remained significantly larger than in controls. CSA of the right coronary artery in patients with aortic valve disease was not different from controls. LV muscle mass was significantly increased in aortic valve disease patients before (364 g) and after (250 g) valve replacement compared with controls (135 g). The appropriateness of coronary artery size with respect to muscle mass was evaluated by normalizing CSA of the left coronary artery (LAD + LCx) per 100 g of LV muscle mass (mm2/100 g). This index amounted to 11 mm2/100 g in controls, to 8 mm2/100 g in preoperative patients (p less than 0.05 versus controls), and to 10 mm2/100 g in postoperative patients with aortic valve disease (p = NS versus controls). CONCLUSIONS: In patients with aortic valve disease, CSA of the proximal LAD and LCx is increased, but this increase is not sufficient to keep CSA per 100 g of LV mass within normal limits. The postoperative decrease in muscle mass is associated with a decrease in the size of LAD and LCx, whereas the size of the right coronary artery remains unchanged. In contrast to the preoperative state, the residually hypertrophied LV myocardium after aortic valve replacement is supplied by an enlarged but adequately sized LAD and LCx.

Aortic Valve↗

PubMed1992

Evaluation of left ventricular segmental wall motion in hypertrophic cardiomyopathy with myocardial tagging.

BACKGROUND: Segmental wall motion was assessed noninvasively in eight patients with hypertrophic cardiomyopathy and six healthy volunteers by magnetic resonance myocardial tagging. METHODS AND RESULTS: Localization scans were performed for determination of the true short-axis views of the left ventricle (double-angulated view). Spatial modulation of magnetization was used to produce a rectangular grid of landmarks. Distortion of the grid was assessed at end diastole, mid systole, and end systole with multiphase gradient echoes. Image sets were acquired at three different planes, namely, the base, the equator, and the apex. Quantitative evaluation was carried out by computer-assisted image analysis. Each individual grid crossing point was identified automatically and the displacement calculated. A polar coordinate system with the center of gravity as motion reference point was chosen to assess fractional rotation and radial displacement at the endocardial, midwall, and epicardial layers of the septal, anterior, posterior, and inferior regions. A wringing motion of the left ventricle with a clockwise rotation of 5.0 +/- 2.4 degrees at the base and a counterclockwise rotation of -9.6 +/- 2.9 degrees at the apex was observed in control subjects. An equal rotation of 5.0 +/- 2.5 degrees at the base and a slightly reduced rotation of -7.3 +/- 5.2 degrees at the apex was found in patients with hypertrophic cardiomyopathy. A transmural gradient in fractional rotation and radial displacement was observed, with the highest values in the endocardial layer. Rotation in patients with hypertrophic cardiomyopathy was significantly less than in normal volunteers in the posterior region of the equatorial and apical planes. Furthermore, radial displacement was significantly reduced in the septum and inferior wall. In the anterior and posterior wall segments, a reduction of the radial displacement was observed only in the epicardium and midwall layers. CONCLUSIONS: Magnetic resonance myocardial tagging allows the noninvasive assessment of regional wall motion. Both in normal volunteers and in patients with hypertrophic cardiomyopathies, cardiac motion occurs in a complex mode, with the base and the apex rotating in opposite directions and the equatorial plane as a transitional zone (wringing motion). A reduced cardiac rotation can be observed in patients with hypertrophic cardiomyopathy mainly in the posterior region, whereas a reduced radial displacement is found in the inferior septal zone.

Adult↗

PubMed1992

Hemodynamic performance and myosin light chain-1 expression of the hypertrophied left ventricle in aortic valve disease before and after valve replacement.

Previously, we have reported on the selective accumulation of an atrial-like myosin light chain-1 (ALC1) in different forms of human ventricular hypertrophy. The present study involves the determination of ALC1 content in a control group and in patients with aortic stenosis or insufficiency before and 56 +/- 23 months after valve replacement and compares the hemodynamic and angiographic parameters. ALC1 was quantified densitometrically after two-dimensional electrophoretic resolution of biopsy specimens from the left ventricle and was expressed in percent of total ventricular light chain-1. The mean ALC1 content was 11.2 +/- 9.2% in preoperative aortic stenosis and 4.5 +/- 1.4% in aortic insufficiency, both being significantly (p less than 0.001) higher than the control value of 0.3 +/- 0.3%. After valve replacement, mean ALC1 content was lower than before, 4.2 +/- 3.3% (p less than 0.05) in stenosis and 3.4 +/- 3.1% (p = NS) in insufficiency. Left ventricular systolic pressure yields a significant (p less than 0.01) linear correlation (r = 0.45) with the ALC1 content in all preoperative and postoperative patients. Patient group averages of ALC1 content correlate directly with left ventricular systolic and end-diastolic pressure and wall thickness (r = 0.94-0.98) and, in an exponential fashion, with peak systolic circumferential wall stress (r = 0.98) but not with muscle mass or any other parameter. The ventricular ALC1 binds to myosin in proportion to its occurrence in the myocardium. The content of the endogenous ventricular light chain-1 did not change under pathological hemodynamics. The response in expression of the ALC1 to pressure and volume overload suggests an adaptational process.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1991

[Diastolic dysfunction].

Diastolic dysfunction is characterized by an abnormal function of one or both ventricles which is manifested by an increased resistance to diastolic filling. The pathophysiology of diastolic dysfunction includes relaxation disturbances, abnormal diastolic filing and/or abnormal passive elastic properties. In 1/5 to 1/3 of all patients with congestive heart failure, diastolic dysfunction is found to be the sole cause of heart failure. The etiology is most commonly severe myocardial hypertrophy and less often coronary artery disease. The prognosis in patients with isolated diastolic dysfunction is good; the annual mortality rate is 8% and 5-year survival approximately 70%. Therapy is based on a reduction of circulating blood volume to reduce diastolic filling pressure and improvement of relaxation and diastolic filling by the administration of calcium antagonists.

Cardiomegaly↗

PubMed1991

Right ventricular systolic function during exercise with and without significant coronary artery disease.

To evaluate the effects of exercise and coronary artery disease on right ventricular (RV) systolic function, rest and exercise biplane RV angiograms were recorded in 20 patients undergoing diagnostic cardiac catheterization. Thirteen patients had exercise angiograms of sufficient quality to undergo analysis and were classified into 2 groups. Group 1 had no or only mild coronary artery disease; group 2 had significant coronary artery disease as manifested by new, exercise-induced, left ventricular regional wall motion abnormalities. RV systolic pressure increased in both groups during exercise: 33 to 57 mm Hg in group 1 (p = 0.0002) and 33 to 55 mm Hg in group 2 (p = 0.0004). Pulmonary resistance did not change in group 1 during exercise but increased in group 2 (3.2 to 4.8 Wood units, p = 0.04). RV ejection fraction increased slightly, but not significantly, during exercise in group 1, but decreased in group 2 (73 vs 58% with exercise [p = 0.01]). The change in RV ejection fraction from rest to exercise correlated closely with the change in pulmonary resistance from rest to exercise (r = -0.89, p less than 0.0001). RV regional wall motion analysis demonstrated a generalized decline in regional ejection fraction in group 2 during exercise, even in patients without right coronary artery disease. In conclusion, there is a decline in RV ejection fraction during exercise in patients with significant coronary artery disease. The generalized reduction in regional RV ejection fraction coupled with the close correlation with the change in pulmonary resistance suggests that increased afterload, rather than RV ischemia, is the cause.

Angiography↗