Active tuberculosis among the inner-city indigent. Perspective on the 1970's.
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Biomedical subjects
Publications and source records attributed to M A Quinones.
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Left ventricular diastolic compliance is determined by the level of operating pressure and the diastolic pressure-volume relation. This relation is curvillinear and the slope of a tangent (operative chamber stiffness) to the pressure-volume curve increases as the chamber progressively fills. Such preload-dependent changes in compliance occur during any acute alteration in ventricular volume. At a given diastolic pressure, operative chamber stiffness (or its reciprocal, operative chamber compliance) is determined by the relative values for ventricular volume and muscle mass and by the stiffness of a unit of myocardium. Thus, there may be a leftward shift of the diastolic pressure-volume curve (increase in the modulus of chamber stiffness) as a consequence of ventricular hypertrophy or an increase in the stiffness of heart muscle itself (increase in modulus of muscle stiffness). To distinguish between hypertrophy and stiff muscle, it is useful to examine the modulus of chamber stiffness, derived from pressure-volume data, together with the volume/mass ratio of the ventricle. In this fashion, changes in the modulus of chamber stiffness that are inappropriate for a given volume/mass ratio may be attributed to changes in the material properties of the heart muscle. Examples of clinical and experimental pressure-volume studies are presented to illustrate the variety of mechanisms by which acute and chronic changes in ventricular chamber compliance evolve during the course of clinical heart disease. The pathophysiology of pulmonary congestion is best understood by considering the factors responsible for producing changes in chamber stiffness of the ventricle, whereas an examination of muscle stiffness is likely to provide more insight into the extent of irreversible functional and structural defects of the myocardium.
The widespread use of organophosphate pesticides creates the possibility of excessive exposure of migrant farm workers to these compounds. Blood cholinesterase determinations were used to compare the organophosphate pesticide exposure of 57 migrant farm workers with that of 35 controls. Frequently reported symptoms of the farm workers which might be related to pesticide exposure were also studied, including headaches, dizziness, loss of weight, nausea, and a general feeling of weakness or loss of energy. Significantly depressed cholinesterase activities were found in the farm workers, with 10.5% of the farm workers having values below the lower limit of normal. There was no significant relationship between frequently reported symptoms of the farm workers and depressed cholinesterase levels.
The temporal relationship between the closure of the aortic valve (AoV) and the onset of the aortic component of the second heart sound (A2) was defined by simultaneous recording of AoV echogram, phonocardiogram (PCG), and electrocardiogram in 25 subjects. Ten subjects had no heart disease (normal); 15 suffered from various cardiac conditions other than AoV disease (patients). The point of coaptation (C) of the AoV cusps to the onset of A2, the C-A2 interval, was measured to the nearest 5 msec. in 125 cycles. Fifty-eight cycles had a C-A2 of 10 msec., and 47 cycles had a C-A2 of 15 msec. The remainder were distributed at intervals below 10 or above 15 msec. The average C-A2 interval was 11.48 +/- 0.38 msec. (mean +/- 1 S.D.). A similar distribution pattern was observed when the total number of cycles was divided into "normal" and "patient" groups. In 3 subjects, simultaneous equisensitive (catheter-tip micromanometer) left ventricular and central aortic pressures, PCG, and AoV echograms were recorded. C-A2 ranged from 0 to 10 msec.; the interval between left ventricular and aortic pressure at the level of the incisura-hangout interval-ranged from 8 to 20 msec. Inhalation of amyl nitrite in one subject produced a significant fall in arterial pressure, accompanied by prolongation of the hangout interval from 10 to 20 msec. and of the C-A2 interval from 0 to 8 msec. Thus, the C-A2 interval is an integral part of the hangout time. Data suggest that A2 does not originate from the coaptation of the aortic valve cusps per se, but is related to events that occur at the time of or slightly after coaptation.
To determine the sensitivity of several isovolumic and ejection phase indices of myocardial contractility to loading, inotropic stimulation and heart rate in man, 14 patients (pts) were studied during cardiac catheterization with simultaneous recordings of left ventricular (LV) pressures and ultrasound dimensions. Measurements were made of instantaneous and mean circumferential fiber shortening velocity (VCF), maximal (max) rate of LV pressure rise (dP/dt), dPHdt divided by end-diastolic circumference [(dP/dt)/C], (DP/dt)/C divided by aortic valve opening pressure [(dP/dt/CP], PEAK CONTRACTILe element velocity (VCE) using total LV pressure, VCE extrapolated to zero total pressure (Vmax), VCE at a developed pressure of 10 mm Hg (VCEDP10) and dP/dt at a common isovolumic developed pressure of 40 mm Hg [(dP/dt)/DP40]. Resulta are expressed in per cent change of the mean for the group. Acute preload increase (8.6% increase in end-diastolic circumference) with volume expansion at constant heart rate in 7 pts produced insignificant changes in VSF, an 8.3% increase in max dP/dt, no change in (dP/dt)/C, a variable response in (dP/dt)/CP, 18% reduction in peak VCE, 16% reduction in Vmax, 14% increase in VCEDP10, and a 10% increase in (dP/dt)/DP40. An acute increase in afterload produced by angiotensin in 8 pts (44% increase in peak stress) led to a 38% decrease in VCF, a 2.5% increase in max dP/dt, no significant change in (dP/dt)/C, a 26% reduction in (dP/dt)/CP, variable responses in peak VCE and Vmax, an 11% increase in VCEDP10 and minor changes in (dP/dt)/DP40. All of the contractility indices were augmented significantly by isoproterenol and atrial pacing. In a given patient, max, dP/dt appears to be useful in the assessment of acute changes in inotropic state since the magnitude of its response to abrupt changes in preload is small and to afterload insignificant. Normalizing max dP/dt for end-diastolic circumference assures better stability during loading with good sensitivity to inotropic stimulation. VCF may be used whenever changes in afterload are minimal. The isovolumic measurements of VCE (regardless of whether total or developed pressure is used) lack sufficient stability during acute changes in loading conditions to warrant their use in the quantitative assessment of acute changes in inotropic state.
A comparison of electrocardiographic manifestations of left atrial enlargement (LAE) and left atrial size by echocardiography was made in 307 patients in sinus rhythm. Electrocardiographic criteria used were L:P wave duration in lead II equal to or greater than 0.12 sec; Va: the ratio of the duration of negative terminal P in V1 to the P-R segment equal to or greater than 1.0; Vb: a negative P terminal force in V1 less than -0.03 mm sec. The echocardiographic diagnosis of left atrial enlargement was based on 1) transverse dimension greater than 4.0 cm; or 2) a ratio of transverse atrial to transverse aortic root dimension greater than 1.17. In the presence of left atrial enlargement, a combination of criteria occurred more often than a single criterion. The overall predictive index of the electrocardiogram for left atrial enlargement was 63% (excluding criterion Vb raised probability to 80%); and that for absence of left atrial enlargement was 78%. The index of coarse versus fine fibrillary waves was unreliable in predicting left atrial enlargement. Changes in P wave morphology may be used as a reasonably specific but less sensitive indicator of left atrial enlargement.
A preliminary survey of circulating vitamin B12 biotin, folate, thiamin, riboflavin, vitamin B6, pantothenate, nicotinate, and vitamin A & B-carotene of 53 Puerto Rican migrant farm workers was undertaken. Results indicate that hypovitaminemia existed particularly for vitamin B12, vitamin B6 and vitamin A.
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Hemodynamic and angiographic data obtained during pain from four patients with Prinzmetal's variant angina are reported. The left ventricular pressure-time index did not increase before or during attacks of angina in three of the four patients; left ventricular systolic performance was impaired during pain in all three. In one of these three patients left ventricular pressure-volume data obtained during angina suggested a reduction in diastolic compliance; in another, pain and S-T segment elevation were present during coronary arterial spasm. The fourth patient had an increase in both arterial blood pressure and heart rate before an attack; in this patient coronary arterial spasm could not be demonstrated during the period of pain and S-T elevation. The data presented suggest that hemodynamic factors that increase the myocardial oxygen requirements are absent and that coronary arterial spasm is present in some, but not all, patients with variant angina.
Two coordinates of left ventricular end-diastolic pressure (P) and volume (V) were provided by the infusion of angiotensin in 22 patients. The slope (k) of the ln P-V relation, coupled with knowledge of the operating (end-diastolic) pressure allows determination of end-diastolic volume compliance (dV/VdP). Estimates of end-diastolic compliance from a single coordinate of pressure and volume compared well (r equals 0.90) with the two coordinate method, whereas for specific compliance (deltaV/V1 deltaP) appeared to be misleading in cases of idiopathic hypertrophic subaortic stenosis and congestive cardiomyopathy. Since volume compliance is determined in part by the operating pressure, compliance may be reduced in small, normal or enlarged ventricles. Left ventricular linear compliance was derived from volume compliance and was normalized for left ventricular wall thickness. The product of linear compliance and end-diastolic stress provides an index of myocardial strain, termed "muscle fiber stretch," which may be related to systolic performance and thus allow comparison of length-performance relations in ventricles with normal and abnormal compliance.
Left ventricular (LV) diastolic pressure (P), volume (V), and rate of change of volume (dV/dt) were determined at 16.7 msec intervals in 17 patients (simultaneous micromanometer and single plane volume angiography). Four patients had mitral stenosis with atrial fibrillation and 13 patients (three normal, two congestive cardiomyophathy, three LV hypertrophy, and five coronary artery disease) were in normal sinus rhythm. Maximum early diastolic filling rates (max dV/dt) in the normal and cardiomyopathy patients were similar and ranged from 269 to 370 cc/m-2/sec; in coronary artery disease and LV hypertrophy, max dV/dt ranged from 197 to 290 cc/m-2/sec and 213 to 255 cc/m-2/sec respectively; in mitral stenosis, max dV/dt ranged from 215 to 270 cc/m-2 sec. The peak filling rate during atrial systole ranged form 60 to 240 cc/m-2/sec in the 13 patients with sinus rhythm. The instantaneous diastolic P-V data were fit by an exponential equation (P = be-kV) and the P-V relation throughout diastole was represented by the best fit line. The rate constant (k) in the equation was highest in the patient with IHSS and lowest in those with large dilated hearts. In mitral stenosis with atrial fibrillation the fit of the equation to the P-V data appeared better than in the patients with normal sinus rhythm. Peak ventricular filling rate during atrial systole varied directly with LV volume distensibility at the onset of atrial systole (r = 0.64). Data suggest that dynamic mechanical properties of the LV influence the diastolic P-V relations and that pressure "deviations" (deltaP) from the best fit line during atrial systole may be related to viscous drag. In a given ventricle the velocity dependence of deltaP appears to be modified by the volume distensibility of the ventricle. Variable rates of filling may preclude the assumption of an exponential relation between P and V throughout diastole and therefore may limit estimates of diastolic distensibility or compliance which rely on such an assumption.
The time course of left ventricular (LV) circumferential stress and fiber shortening velocity (Vcf) were determined at 20 msec intervals in 30 patients from simultaneous recordings of LV pressure (micromanometer) and LV dimensions (echography). In 12 patients with normal LV function, endocardial and midwall maximal (max) Vcf, Vcf at peak stress, and endocardial mean Vcf were significantly greater than in eight patients with myocardial disease. Peak stress was less in the normal subjects (mean equal 241 gl/cm2, range 180 to 310 g/cm2) than in those with myocardial diseases (mean equals 371 g/cm2, range 280 to 513 g/cm2). Vcf was reduced in five out of seven patients with chronic LV volume overload, while peak stress ranged from normal in three to increased in four. Max Vcf, mean Vcf, and peak stress were normal in three patients with chronic LV pressure overload; Vcf at peak stress was normal in two. Good correlation was observed between angiographic determinations of mean Vcf and endocardial max Vcf, Vcf at peak stress and mean Vcf. Induced changes in preload in five patients (dextran infusion at constant heart rate) produced a 12.2 per cent increase in peak stress (P small than 0.05), and insignificant changes in max Vcf (3.7 per cent increase, P = NS), in Vcf at peak stress (5 per cent decrease, P smaller than 0.05), in mean Vcf (0.7 per cent increase, P = NS). Increasing afterload with angiotensin in seven patients (peak stress increased by 45 per cent, P smaller than 0.01) reduced max Vcf, Vcf at peak stress and mean Vcf by 33 per cent, 39 per cent respectively. Lowering afterload in one patient (amyl nitrite) produced an increase in Vcf. Improvement in Vcf was observed in all instances during positive inotropic stimulation (isoproterenol in three normals, digoxin in four with myocardial disease). Thre response of endocardial and midwall Vcf to loading and contractility were similar. In man Vcf is an index of myocardial contractility which is affected minimally by changes in preload but responds inversely to changes in afterload. Its sensitivity to acute afterload changes may, at times, limit its clinical applicability.
The Civil War (1861-1865) has long been blamed as the catalyst for the spread of drug addiction in America. This paper attempts to examine this hypothesis through an extensive review of pertinent literature, and to clarify misconceptions concerning addiction problems associated with the war.
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