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Biomedical subjects

L P McLaurin

Publications and source records attributed to L P McLaurin.

At least 19 recordsLinked to original sources
PubMed1980

Noninvasive assessment of pulmonary hypertension from right ventricular isovolumic contraction time.

In order to assess a noninvasive method of predicting pulmonary arterial pressure in adults, right ventricular systolic time intervals were determined with echocardiography simultaneously with pulmonary arterial end-diastolic pressure measurements. Right ventricular isovolumic contraction time was measured from echographic recordings of the tricuspid and pulmonary valves. Although this interval was found to increase as pulmonary arterial pressure increased, the method cannot be used to predict quantitatively the level of pulmonary arterial pressure in adults. However, an echocardiographically determined right ventricular contraction time of less than 25 ms suggests a normal pulmonary arterial pressure. In patients with pulmonary parenchymal diseases, echograms of the tricuspid and pulmonary valves are only rarely of such quality as to permit accurate delineation of the valvular events required for these measurements.

Adolescent↗
PubMed1980

Psychosocial outcome after coronary artery surgery.

To describe psychosocial adaptation after coronary artery surgery and to identify preoperative factors associated with good outcome, the authors interviewed 30 patients before and 1--2 years after surgery. Despite good physiologic outcome (as measured by treadmill and cardiac function) this sample was found to be functioning poorly. Eighty-three percent were unemployed, and 57% were sexually impaired. A preoperative duration of symptoms of eight months or more was associated with significantly worse postoperative overall adaptation. Most patients who had suffered angina eight months or longer evidenced a damaged self-concept, which was reinforced rather than repaired by the experience of surgery.

Angina Pectoris↗
PubMed1977

Effect of angina on the left ventricular diastolic pressure-volume relationship.

The increased left ventricular end-diastolic pressure associated with myocardial ischemia was studied in 19 patients at cardiac catheterization. Single plane left ventriculograms were performed using high fedelity micromanometer tipped catheters before and immediately following rapid atrial pacing. Left ventricular diastolic properties were evaluated by constructing diastolic pressure-volume curves from the simultaneous pressure and volume data. In seven control patients, there was no significant change in left ventricular hemodynamics or the diastolic pressure-volume curve after atrial pacing. Twelve patients with significant coronary artery disease developed angina during pacing and had an increased left ventricular end-diastolic pressure (18 +/- 2 mm Hg, control, vs 30 +/- 2 mm Hg, angina, P less than .01) in the immediate post-pacing period. In these patients, the post-pacing ejection fraction was modestly decreased (0.63 +/- 0.03, control, vs 0.57 +/- 0.03, angina P less than 0.01), and left ventricular volumes at end systole (59 +/- 8 cc, control, vs 74 +/- 9 cc, angina, P less than 0.0125) were increased. The post-pacing diastolic pressure-volume curves in all 12 patients were shifted upward as compared with control so that for any given diastolic volume, pressure was higher during angina. The data indicate that the increased left ventricular diastolic pressure during myocardial ischemia is the result of both impaired left ventricular systolic performance and altered left ventricular diastolic properties.

Adult↗
PubMed1977

Contractile state of the left ventricle in man as evaluated from end-systolic pressure-volume relations.

End-systolic pressure (PES), volume (VES), wall tension (TES) and circumference (CES) of the human left ventricle were studied at cardiac catheterization in 24 subjects with varying degrees of left ventricular dysfunction. Acute alterations in systolic load consistently resulted in changes in VES and CES, with a smaller volume and circumference characterizing the lower systolic load in each subject. End systolic pressure-volume lines were constructed by plotting PES against VES at the higher and lower systolic load in each subject. The slope of the resultant lines was considerably steeper for normal than for poorly contractile left ventricles. Vo, the volume axis intercept of the line (i.e., the theoretical VES at PES = O) was significantly smaller for normal than for poorly contractile ventricles. Similar findings were noted for Co, the theoretic end-systolic circumference at zero end-systolic ventricular wall tension. Post-extrasystolic potentiation resulted in decreased VES and CES with no change in PES and only a slight fall in TES. In conclusion, end-systolic pressure-volume and tension-circumference relations reflect the contractile state of left ventricular myocardium. Quantitation of these relationships may provide a useful new approach to the assessment of myocardial function in man.

Blood Pressure↗
PubMed1977

Effects of sodium nitroprusside on left ventricular diastolic pressure-volume relations.

The effect of sodium nitroprusside on the relationship between left ventricular pressure and volume during diastole was studied in 11 patients with congestive heart failure. Nitroprusside was infused to lower mean arterial pressure approximately 20-30 mm Hg. High fidelity left ventricular pressures were recorded in all patients simultaneously with left ventricular cineangiography (biplane in eight and single plane in three patients), allowing precise measurement of pressure and volume throughout the cardiac cycle. Left ventricular diastolic pressure-volume curves were constructed in each patient from data obtained before and during nitroprusside infusion. In 9 of 11 patients there was a substantial downward displacement of the diastolic pressure-volume curve during nitroprusside infusion, with left ventricular pressure being lower for any given volume with nitroprusside. Serial left ventricular cineangiograms performed 15 min apart in six additional subjects who did not receive sodium nitroprusside showed no shift in the diastolic pressure-volume relation, indicating that the shift seen with nitroprusside was not due to the angiographic procedure itself. A possible explanation for the altered diastolic pressure-volume relationships with nitroprusside might be a direct relaxant effect of nitroprusside on ventricular muscle, similar to its known relaxant effect on vascular smooth muscle. Alternatively, nitroprusside may affect the diastolic pressure-volume curve by affecting viscous properties or by altering one or more of the extrinsic constraints acting upon the left ventricle.

Aorta↗
PubMed1977

The clinical recognition of congestive heart failure.

The recognition of early or mild congestive heart failure in the ambulatory patient is a common clinical challenge in everyday practice. Early diagnosis requires attention to symptoms, signs, and radiographic changes which may be minimal. This paper reviews basic pathophysiological principles involved in congestive heart failure and summarizes etiological factors which may cause or precipitate congestive heart failure. The symptoms, signs, and subtle radiological findings of early congestive heart failure are also described in some detail.

Cough↗
PubMed1976

Combined hemodynamic-ultrasonic method for studying left ventricular wall stress: comparison with angiography.

Calculation of left ventricular wall stress in man has traditionally required angiographic and left ventricular pressure measurement, making study of interventions difficult. We have developed a combined hemodynamic-ultrasonic technique for measuring left ventricular meridional wass stress (sigma m) throughout the cardiac cycle. Simultaneous measurements of left ventricular pressure, ultrasonically determined wall thickness (h[echo]), and minor axis (D[echol]) were made during cardiac catheterization in nine subjects, three with chronic left ventricular pressure overload, four with left ventricular volume overload and two with normal left ventricular function. Within 30 minutes, left ventricular cineangiography was performed in each subject and angiographic wall thickness (h[angio]) and minor axis (D[angio]) were measured. Comparison of values for each subject throughout the cardiac cycle (average 18 data points/cycle) yielded close correlation: For D(echo) versus D(angio), r values ranged from 0.82 to 0.98 whereas for h(echo) versus h(angio), r values ranged from 0.56 to 0.98 for the nine subjects. Meridional wall stress was calculated after the method of Sandler and Dodge as PRi2/h(2Ri + h), where Ri equals the inner wall radius, calculated as D/2 for both ultrasonic and angiographic methods. Agreement between ultrasonic and angiographic methods was excellent in each subject, with close superimposition of the stress-time plots constructed by the different techniques. In summary, a new method for measurement of left ventricular wall stress has been developed and validated by comparison with an angiographic reference standard. This method has potential advantages, including the ability to study meridional wall stress continuously and to assess its response to serial interventions.

Cineangiography↗
PubMed1976

Clinical evaluation of the Lillehei-Kaster pivoting-disc valve.

A four-year clinical evaluation of 133 patients with Lillehei-Kaster pivoting-disc valves has shown that patients with an aortic valve prosthesis have remained free from valve-related problems. Patients with a mitral valve implanted have a satisfactory survival record as calculated by actuarial methods; however, a 10% incidence of valve thrombosis was experienced. Analysis suggests that this may be related to inadequate anticoagulation or use of an inappropriate suturing technique or both. The patients enjoyed significant clinical improvement following operation, with no evidence of hemolysis. A history suggestive of postoperative embolization was present in only 1 patient in this series.

Adolescent↗
PubMed1976

An echocardiographic study of the interventricular septum in constrictive pericarditis.

Ten patients with constrictive pericarditis were studied echocardiographically with specific reference to inter-ventricular septal dynamics. Abnormal movement of the interventricular septum was present in 8 patients and consisted of flattening in systole and unusual posterior motion in diastole. The aetiology of this type of movement is at present unknown but may be related to restriction of normal cardiac rotational dynamics. The interventricular septum also showed diminished degree of thickening (mean 21-2%). The amplitude of excursion was generally at the upper limit of or greater than normal. Left ventricular posterior wall amplitude of excursion was normal. Flattening of left ventricular posterior wall diastolic movement was seen in 4 patients. Right ventricular end-diastolic dimension was slightly increased (1-2 to 1-7 cm/m2) in 5 of 8 patients with abnormal septal motion, but no haemodynamic evidence of diastolic volume overload was found. Posterior pericardial thickening was noted echocardiographically when posterior calcification was present. We conclude that the most common though non-specific feature of the echocardiogram in patients with constrictive pericarditis is abnormal septal motion. Flattening of left ventricular posterior wall diastolic movement, posterior pericardial thickening, and epicardial-pericardial separation may also occur.

Adult↗
PubMed1976

Diastolic properties of the left ventricle.

Left ventricular pressure and volume during diastole reflect the interaction of ventricular elastic, viscous, and inertial properties, and the completeness of myocardial relazation. Myocardial relaxation may be impaired in the acutely ischemic ventricle, partly accounting for the abnormal diastolic pressure-volume relation in this condition. Altered elasticity of its wall can cause increased stiffness of the ventricular chamber, as in aortic stenosis, coronary heart disease, and infiltrative cardiomyopathies. In aortic stenosis, increased left ventricular stiffness results in an increase in pressure increment associated with left atrial contraction. Generation of such a high filling pressure is critical in maintaining adequate end diastolic sarcomere stretch in the left ventricle and probably accounts for the frequent deterioration of patients with aortic stenosis after development of atrial fibrillation or nodal rhythm. Many signs and symptoms of cardiac failure, previously attributed to impaired systolic performance, may be due to partly to altered diastolic properties of the ventricular chambers.

Animals↗
PubMed1975

Wall stress and patterns of hypertrophy in the human left ventricle.

It is generally recognized that chronic left ventricular (LV) pressure overload results primarily in wall thickening and concentric hypertrophy, while chronic LV volume overload is characterized by chamber enlargement and an eccentric pattern of hypertrophy. To assess the potential role of the hemodynamic factors which might account for these different patterns of hypertrophy, we measured LV wall stresses throughout the cardiac cycle in 30 patients studied at the time of cardiac catheterization. The study group consisted of 6 subjects with LV pressure overload, 18 with LV volume overload, and 6 with no evidence of heart disease (control). LV pressure, meridional wall stress (sigman), wall thickness (h), and radius (R) were measured in each patient throughout the cardiac cycle. For patients with pressure overload, LV peak systolic and end diastolic pressures were significantly increased (220 plus or minus 6/23 plus or minus 3 mm Hg) compared to control (117 plus or minus 7/10 plus or minus 1 mm Hg, P less than 0.01 for each). However, peak systolic and end diastolic (sigman) were normal (161 plus or minus 24/23 plus or minus 3 times 10-3 dyn/cm-2) compared to control (151 plus or minus 14/17 plus or minus 2 times 10-3 dyn/cm-2, NS), reflecting the fact that the pressure overload was exactly counterbalanced by increased wall thickness (1.5 plus or minus 0.1 cm for pressure overload vs. 0.8 plus or minus 0.1 cm for control, P less than 0.01). For patients with volume overload, peak systolic (sigman) was not significantly different from control, but end diastolic (sigmam) was consistently higher than normal (41 plus or minus 3 times 10-3 dyn/cm-2 for volume overload, 17 plus or minus 2 times 10-3 dyn/cm-2 for control, P less than 0.01). LV pressure overload was associated with concentric hypertrophy, and an increased value for the ratio of wall thickness to radius (h/R ratio). In contrast, LV volume overload was associated with eccentric hypertrophy, and a normal h/R ratio. These data suggest the hypothesis that hypertrophy develops to normalize systolic but not diastolic wall stress. We propose that increased systolic tension development by myocardial fibers results in fiber thickening just sufficient to return the systolic stress (force per unit cross-sectional area) to normal. In contrast, increased resting or diastolic tension appears to result in gradual fiber elongation or lengthening which improves efficiency of the ventricular chamber but cannot normalize the diastolic wall stress.

Adolescent↗
PubMed1975

Reduced systemic vascular resistance as therapy for severe mitral regurgitation of valvular origin.

We examined the hemodynamic response to afterload reduction by sodium nitroprusside in 7 patients with severe mitral regurgitation of purely valvular origin. Lowering of systemic vascular resistance was associated with major reductions in pulmonary capillary mean (29 +/- 2 to 13 +/- 1 mm Hg) and left ventricular end diastolic (20 +/- 3 to 9 +/- 1 mm Hg) pressures, while substantial increases were noted in cardiac index (2.2 +/- 0.5 to 3.1 +/- 0.4 litres/min per m2 body surface area) and forward stroke volume (23 +/- 4 to 34 +/- 4 ml/beat/m2 body surface area). Angiographic calculations showed significant decreases in regurgitant volume (73 +/- 19 to 55 +/- 12 ml/beat/m2 body surface area) and regurgitant fraction (0.70 +/- 0.07 to 0.57 +/- 0.06). No significant change occurred in left ventricular ejection fraction or heart rate, suggesting that the improved cardiac function was not due to a reflex increase in adrenergic stimulation. These observations support the concept that afterload reduction may be therapeutic in severe mitral regurgitation by reducing impedance to forward left ventricular output, thereby promoting greater forward and small regurgitant fractions of the total stroke volume.

Adult↗