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Biomedical subjects

W C Little

Publications and source records attributed to W C Little.

At least 55 records · Page 3Linked to original sources
PubMed1994

Effect of adenosine on contractile state and oxygen consumption in isolated rat hearts.

We studied the effects of adenosine on oxygen consumption and contractile state in 17 isolated, crystalloid-perfused, isovolumically contracting rat heart preparations at constant coronary flow. In 10 experiments we determined adenosine-contractile state dose-response relationships in three groups of hearts using two different perfusates and in the presence and absence of adrenergic blockade. Adenosine consistently reduced contractile state in a dose-dependent fashion, reducing the ventricular pressure developed at a constant ventricular volume by 24% on average at its maximal effect. An adenosine concentration of 111 microM on average produced 50% of the maximal effect. In seven experiments we determined the end-systolic pressure-volume and oxygen consumption-pressure-volume area (MVO2-PVA) relationships at two calcium concentrations (1.5 and 0.75 mM) and with adenosine 400 microM (1.5 mM Ca2+). Contractile state was indexed by the developed pressure at a ventricular volume of 0.3 ml (P0.3). Compared with 1.5 mM Ca2+, mean P0.3 was reduced by 38% with 0.75 mM Ca2+ and by 18% with adenosine. Whereas the MVO2-PVA slopes did not change, the mean MVO2 intercept was reduced by 22% with 0.75 mM Ca2+ and by 13% with adenosine. The MVO2 intercept, which represents the oxygen consumed by the unloaded heart, was directly related to P0.3. This relationship, which represents the oxygen cost of contractility, was not affected by adenosine. We conclude that at constant coronary flow and perfusion pressure adenosine reduces myocardial contractility and the oxygen consumed for excitation-contraction coupling. However, adenosine does not affect the slope of the MVO2-PVA relation or the oxygen cost of contractility.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1994

Relation between left ventricular oxygen consumption and pressure-volume area in conscious dogs.

BACKGROUND: The relation between left ventricular (LV) oxygen consumption (MVO2) and pressure-volume area (PVA) developed in isolated hearts provides a powerful method to understand cardiac energetics. We investigated application of this relation to the intact circulation, determining its response to steady-state and transient load alterations and enhanced contractility in conscious animals. METHODS AND RESULTS: Eight dogs were instrumented to measure LV pressure (micromanometer), LV volume (three sonomicrometers), and left circumflex and anterior descending coronary artery flows (ultrasonic flowmeter). Data were acquired after recovery from the surgery with the animals awake and unsedated. After administration of hexamethonium and atropine, steady-state loading conditions were changed with phenylephrine or nitroprusside in four to five steps before and during the infusion of dobutamine (6 to 10 micrograms.-1kg.-1min). MVO2 and PVA obtained under steady-state conditions were linearly correlated both before and during dobutamine. The MVO2-PVA relation obtained on a beat-to-beat basis during transient caval occlusion was less linear and not coincident with the steady-state relation. Dobutamine shifted the steady-state MVO2-PVA relation upward in all hearts, increasing the MVO2 axis intercept of the MVO2-PVA relation (P < .01). This intercept correlated with ventricular contractility assessed by the slope (Ees) of the LV end-systolic pressure-volume relation determined by caval occlusion (r = .76, P < .05). The slope of the MVO2-PVA relation increased with dobutamine in seven of eight animals, with the inverse of the slope (representing contractile efficiency) being 31 +/- 6% during control and 24 +/- 6% after dobutamine (P = .06). CONCLUSIONS: MVO2 and PVA are linearly related during steady-state alterations in loading conditions in conscious dogs but not on a beat-by-beat basis during transient caval occlusion. Increase in contractility by dobutamine produces an upward shift of the MVO2-PVA relation.

Animals↗
PubMed1994

Mechanism of altered patterns of left ventricular filling during the development of congestive heart failure.

BACKGROUND: The mechanism of the alterations in the pattern of left ventricular (LV) filling during the development of congestive heart failure (CHF) is not fully understood. METHODS AND RESULTS: We studied six conscious dogs instrumented to measure LV and left atrial (LA) pressures and LV volume as CHF was induced by rapid pacing. Diastolic filling dynamics were serially measured over 4 weeks during normal sinus rhythm. Four days after we initiated pacing, the peak early diastolic filing rate decreased from 108 +/- 24 to 88 +/- 27 mL/s (P < .05) as the maximal early diastolic LA-LV pressure gradient decreased associated with a slowing of the rate of LV relaxation. Subsequently, the peak early filling rate progressively increased, returning to control at 1 week, and by the fourth week, it had increased to 168 +/- 39 mL/s (P < .05). These changes in early filling rates occurred as the maximal early diastolic LA-LV pressure gradient increased in association with a progressive increase in LV pressure despite further progressive slowing of the rate of LV relaxation. Throughout the development of CHF, peak early filling rate and the maximal LA-LV pressure gradient correlated (r = .99, P < .001). The early filling deceleration rate increased and deceleration time progressively decreased over the 4 weeks as LV stiffness and net LA plus LV stiffness increased (P < .05). As predicted by a theoretical analysis, the deceleration time was linearly related to the reciprocal of the square root of LV stiffness (r = .94, P < .01). CONCLUSIONS: Early in CHF, slowing of LV relaxation reduces the maximal early diastolic LA-LV pressure gradient, decreasing the peak early filling rate. As CHF progresses, this is overcome by an increase in LA pressure that augments the early diastolic LA-LV pressure gradient, increasing peak early filling rate. Increasing LV stiffness during the development of CHF progressively shortens the early filling deceleration time and augments the early filling deceleration rate. These observations suggest that the early filling deceleration time reflects LV stiffness.

Animals↗
PubMed1994

Effect of exercise on left ventricular mechanical efficiency in conscious dogs.

BACKGROUND: We studied the effect of exercise (7.2 to 8.0 km/h) on the efficiency of the conversion of metabolic energy to external work or stroke work (SW) by the left ventricle (LV). METHODS AND RESULTS: Energy use was calculated from LV myocardial oxygen consumption per beat (MVO2). LV volume was calculated from orthogonal dimensions and coronary flow measured with ultrasonic flow probes. The total mechanical energy of the LV was calculated as the pressure-volume area (PVA). At rest, the MVO2-PVA point fell on the MVO2-PVA relation determined by steady-state changes in arterial pressure produced by graded infusions of phenylephrine. Exercise increased the slope (Ees) of LV end-systolic pressure-volume (PV) relation by 29%. During exercise, the MVO2-PVA point shifted to the right only slightly above the control MVO2-PVA relation by 0.007 +/- 0.005 mL O2.beat-1.100 g LV-1. Despite the increase in ventricular contractility with exercise, the PVA/MVO2 ratio was unchanged because of the marked increase in PVA. During exercise, the transmission of total mechanical energy to external work (SW/PVA) increased from 65 +/- 5% to 72 +/- 4% (P < .01) as the ratio of the arterial end-systolic elastance to Ees decreased from 1.1 +/- 0.2 to 0.8 +/- 0.1 (P < .05). Thus, LV mechanical efficiency (SW/MVO2 = SW/PVA.PVA/MVO2) improved from 12.9 +/- 1.5% to 14.3 +/- 1.1% (P < .05) during exercise. CONCLUSIONS: Exercise increases the efficiency of conversion of metabolic energy to external work by the LV due to alteration in LV arterial coupling resulting in increased production of mechanical energy and enhanced transmission of mechanical energy to external work, which more than offsets any increased metabolic cost of the enhanced contractility.

Animals↗
PubMed1994

Vascular versus myocardial effects of calcium antagonists.

As vascular smooth muscle tone and myocardial contractility both depend on calcium entry, the calcium antagonists are not only potent arterial vasodilators, but may also have important negative inotropic effects. For example, verapamil is nearly equipotent in reducing vascular smooth muscle tone and myocardial contraction in isolated tissue preparations. In contrast, felodipine has high vascular selectivity in such preparations, and drug concentrations required to depress myocardial contraction are more than 100 times greater than those required to relax vascular smooth muscle. In the isolated, isovolumetrically contracting canine left ventricle, clinically relevant concentrations of felodipine (14 nmol/L) produce coronary vasodilation and a mild positive inotropic response. Using left ventricular (LV) pressure-volume analysis, we evaluated a similar dose of felodipine (plasma drug concentration 16 nmol/L) in conscious dogs. Felodipine produced a 25mm Hg fall in arterial pressure and a 10% reduction in peripheral vascular resistance. There was no negative inotropic effect. Instead, myocardial contractile performance was slightly but significantly enhanced. These results were not altered by adrenergic blockade. Further studies in our laboratory showed that doses of amlodipine and nifedipine producing arterial vasodilation of a magnitude similar to that produced by felodipine had negative inotropic effects in the conscious dog. Only felodipine enhanced the rate of LV relaxation and the rate of early diastolic filling. Thus, felodipine was significantly more vasoselective than amlodipine and nifedipine. The direct inotropic effects of calcium antagonists are difficult to evaluate in clinical studies because of the load-dependence of most conventional measures of LV performance. However, no negative inotropic effects are clinically relevant doses of felodipine have been identified.(ABSTRACT TRUNCATED AT 250 WORDS)

Amlodipine↗
PubMed1994

Effects of felodipine on left ventricular systolic and diastolic performance in congestive heart failure.

We studied the effects of a dihydropyridine calcium blocker, felodipine, on left ventricular (LV) contractile performance and diastolic filling dynamics in conscious dogs with pacing-induced congestive heart failure (CHF) before and after autonomic blockade. Eleven conscious dogs were instrumented to measure micromanometer LV and left atrial (LA) pressure (P) and to determine LV volume (V) from three dimensions. CHF was induced by 4 to 5 weeks of right ventricular pacing. After CHF, the mean LV end-diastolic (ED) P increased (9.7 +/- 2.9 vs. 27.9 +/- 6.8 mm Hg, P < .05), LVEDV and end-systolic (ES) V increased and stroke volume (SV) decreased (15.3 +/- 2.4 vs. 9.6 +/- 3.0 ml, P < .05). The time constant of LV relaxation (T) (25.9 +/- 2.9 vs. 37.9 +/- 5.1 msec, P < .05) and LVES wall stress (WS) (63.4 +/- 21.0 vs. 74.6 +/- 23.7 g/cm2, P < .05) also increased. After CHF, felodipine (25 nmol/kg i.v., plasma concentrations 17.4 +/- 3.2 nmol/L) produced significant decreases in LVESP (119 +/- 12 vs. 96 +/- 11 mm Hg, P < .05), arterial elastance, total systolic resistance (TSR) (0.11 +/- 0.04 vs. 0.07 +/- 0.03 mm Hg/ml/min, P < .05) and LVESWS (74.6 +/- 23.7 vs. 60.2 +/- 17.3 g/cm2, P < .05). Felodipine increased the slopes of the ESP-V relation (5.6 +/- 1.5 vs. 7.8 +/- 0.7 mm Hg/ml, P < .05), the dP/dtmax-EDV relation (51.4 +/- 6.1 vs. 85.3 +/- 10.1 mm Hg/ml sec, P < .05) and the stroke work-EDV relation (69.8 +/- 7.1 vs. 78.9 +/- 7.1 mm Hg, P < .05) and shifted all three relations to the left, indicating enhanced contractile performance.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Comparison of effects of dihydropyridine calcium antagonists on left ventricular systolic and diastolic performance.

We compared the effects of three dihydropyridine calcium antagonists (felodipine, nifedipine and amlodipine) on left ventricular (LV) contractile performance and diastolic filling dynamics in eight conscious animals. After administering metoprolol and atropine, felodipine (25 nmol/kg i.v.) produced significant decreases in LV end-systolic pressure (PES) (109 +/- 15 vs. 88 +/- 12 mmHg, P < .05) and arterial elastance (Ea) (12.6 +/- 4.5 vs. 8.5 +/- 3.4 mmHg/ml, P < .05), whereas the heart rate was unchanged. Felodipine increased the slopes of the end-systolic P-V relation (7.4 +/- 0.9 vs. 9.9 +/- 1.0 mmHg/ml, P < .05), the dP/dtmax-end diastolic volume (VED) relation (68.1 +/- 11.2 vs. 94.9 +/- 14.3 mmHg/sec/ml, P < .05), and the stroke work (SW)-VED relation (72.1 +/- 3.1 vs. 82.8 +/- 5.2 mmHg, P < .05), and shifted all three relations to the left, indicating enhanced contractile performance. In contrast, at doses that produced equivalent reductions of PES, nifedipine (375 nmol/kg i.v.) and amlodipine (780 nmol/kg i.v.), significantly decreased the slopes of the end-systolic P-V relation, the dP/dtmax-VED relation and the SW-VED relation and shifted all three relations to the right, indicating depressed LV contractile performance. Felodipine decreased the time constant (T) of LV relaxation (32.2 +/- 5.2 to 28.8 +/- 5.2 msec, P < .05) and increased the maximum rate of early diastolic LV filling (dV/dtmax) (167 +/- 22 to 207 +/- 26 ml/sec, P < .05). Amlodipine had the opposite effect, slowing T (31.0 +/- 4.9 to 33.9 +/- 5.4 msec, P < .05) and decreasing dV/dtmax (173 +/- 39 to 154 +/- 30 ml/sec, P < .05), whereas nifedipine had no significant effects on T, PGmax or dV/dtmax. Thus, we conclude that in conscious dogs after autonomic blockade, at dosages that produced equivalent arterial vasodilation, felodipine augmented, whereas amlodipine depressed, LV contractile performance, LV relaxation and early LV filling. Nifedipine decreased LV contractile performance but had no significant effect on LV relaxation and early LV filling.

Amlodipine↗
PubMed1993

Should patients with heart disease exercise in the morning or afternoon?

OBJECTIVE: To compare the cardiovascular risk of exercise in the morning and afternoon in patients with established heart disease. DESIGN: Retrospective cohort study. PATIENTS: Patients with established heart disease referred for participation in a comprehensive cardiac rehabilitation program. INTERVENTION: Supervised, submaximal exercise (1 hour three times per week) performed either in the morning (7:30 AM) or the afternoon (3 PM). MAIN OUTCOME: Documented cardiac events that occurred while patients were exercising in the rehabilitation programs. RESULTS: There were five cardiac events in 168,111 patient-hours of exercise in the morning, with an incidence of 3.0 +/- 1.3 events per 100,000 patient-hours. There were two events during the 84,491 patient-hours of exercise in the afternoon, for an incidence of 2.4 +/- 1.5 events per 100,000 patient-hours (not significant). The risk ratio of cardiac events during exercise in the morning compared with the afternoon was 1.27 (95% confidence interval, 0.25 to 6.55). CONCLUSION: In patients with coronary artery disease, the incidence of cardiac events is low during regular, submaximal exercise whether performed in the morning or the afternoon.

Adult↗
PubMed1993

Characteristics of single isovolumic left-ventricular pressure waves of dog hearts in situ.

By fitting isovolumic phases of an ejecting beat with a model-wave function, one can predict source pressure of the ejecting beat (Sunagawa et al. Trans Biomed Eng 1980; 27:299-305), this being a major determinant of systolic performance. Prior applications of this principle have involved two assumptions: (1) that the isovolumic pressure wave is shaped like an inverted cosine wave, and (2) that duration of an isovolumic beat is the same as that of an ejecting beat. The first assumption might cause overestimation of source pressure, since an isovolumic pressure wave begins declining before the midpoint of the wave. The second assumption might cause underestimation of source pressure, since an ejecting beat is always shorter than an adjacent isovolumic beat at the ejecting beat's end-diastolic volume. Although the two errors tend to cancel, it would be more rational and accurate to use a realistic model wave shape and a realistic isovolumic beat duration. To acquire the information necessary for this, pressure and volume time courses were measured during ejecting beats and adjacent isovolumic beats in dogs under the following steady-state conditions: basal, atrial pacing at various rates, infusion of dobutamine, infusion of verapamil, coronary ligation(s), and ventricular pacing at various sites. These conditions affected the amplitude and duration of isovolumic pressure waves substantially but did not affect the shape of the waves significantly. The duration of each isovolumic beat exceeded that of the previous ejecting beat to a degree which corresponded approximately to the ejecting beat's normalized pressure reserve (source pressure minus peak ejection pressure)/(source pressure). A more accurate source-pressure prediction should be possible by use of a realistic isovolumic pressure-wave shape and by taking account of the effect of pressure reserve on contraction duration.

Animals↗
PubMed1993

Congestive heart failure: systolic and diastolic function.

There is increasing recognition that disorders of both left ventricular systolic and diastolic function can result in congestive heart failure. As such, consideration of both the filling and emptying characteristics of the left heart is needed to evaluate the hemodynamic abnormalities present in this syndrome. Considerations of the systolic (emptying) and diastolic (filling) pumping characteristics of the left heart also provides a conceptual basis to classify and understand the pathophysiology of congestive heart failure. In this context, systolic dysfunction can be defined as impaired emptying of the LV, apparent as a decreased (< 50%) effective ejection fraction (forward stroke volume divided by end-diastolic volume). Systolic dysfunction may result from impaired myocardial contractile function, increased left ventricular afterload, and/or structural abnormalities of the left heart. Diastolic dysfunction can be defined as a condition in which filling of the LV sufficient to produce an adequate cardiac output requires an elevated pulmonary venous pressure. Thus, diastolic dysfunction is clinically manifested as pulmonary congestion. Defined in this manner, the most common cause of diastolic dysfunction is systolic dysfunction. In fact, the most common symptom of patients with systolic dysfunction is dyspnea from the resulting diastolic dysfunction. Diastolic dysfunction in the setting of normal systolic function may be due to obstruction of left ventricular filling, impaired left ventricular distensibility, or extensive external compression of the LV. Treatment of diastolic dysfunction can be accomplished by relieving myocardial ischemia, improving systolic function, lowering arterial systolic pressure, and decreasing cardiac distention.

Cardiac Output↗
PubMed1993

Effect of vasopressin on left ventricular performance.

We assessed the effect of arginine vasopressin (AVP) on left ventricular (LV) performance in eight conscious dogs. Five minutes after AVP infusion (6 microns.kg-1 x min-1 for 2 min) the plasma AVP was elevated from 3.9 +/- 0.9 to 14.7 +/- 4.6 pg/ml (P < 0.05). With all reflexes intact, AVP caused significant increases in LV end-systolic pressure (P) (112 +/- 8 vs. 122 +/- 7 mmHg, P < 0.05) end-systolic volume (V) (30 +/- 5.8 vs. 38 +/- 7.7 ml, P < 0.05), total systemic resistance (6.2 +/- 1.8 vs. 10.6 +/- 4.0 mmHg.dl-1 x min, P < 0.01) and arterial elastance (Ea) (6.8 +/- 3.0 vs. 8.6 +/- 3.9 mmHg/ml, P < 0.05), while the heart rate (110 +/- 6 vs. 82 +/- 10 beats/min, P < 0.05) and stroke volume (16.5 +/- 4.3 vs. 14.2 +/- 3.9 ml, P < 0.05) were decreased. There was no significant change in the coronary sinus blood flow (82 +/- 19 vs. 78 +/- 22 ml/min, P = not significant). AVP decreased the slopes of LV end-systolic P-V relation (10.7 +/- 1.1 vs. 8.1 +/- 1.9 mmHg/ml, P < 0.05), the maximal first derivative of LV pressure (dP/dtmax)-end-diastolic volume (VED) relation (135.2 +/- 18.7 vs. 63.1 +/- 7.7 mmHg.s-1 x ml-1, P < 0.05), and the stroke work-VED relation (81.1 +/- 4.1 vs. 66.7 +/- 2.8 mmHg, P < 0.05) and shifted the relations to the right, indicating a depression of LV performance. A similar increase in Ea produced by methoxamine did not depress LV performance.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Effect of exercise on left ventricular-arterial coupling assessed in the pressure-volume plane.

The left ventricle (LV) and arterial system are nearly optimally coupled to produce stroke work (SW) at rest. However, the effect of exercise on the coupling between the LV and arterial system has not been directly determined. We evaluated 11 dogs who were instrumented to determine LV volume from three diameters. The LV end-systolic pressure (Pes)-volume (Ves) relation was determined by transient caval occlusion at rest and while the animals ran at 5-7 mph on a treadmill. During exercise, the Pes-Ves relation was shifted toward the left and the slope [end-systolic elastance (Ees)] increased from 7.7 +/- 2.8 to 12.7 +/- 4.2 (SD) mmHg/ml (P < 0.05). The arterial end-systolic elastance (Ea), calculated as Pes divided by stroke volume, increased during exercise (8.8 +/- 3.0 to 10.9 +/- 4.7 mmHg/ml, P < 0.05). The ratio of Ees to Ea increased during exercise from 0.89 +/- 0.31 to 1.27 +/- 0.12 (P < 0.05). The portion of the pressure-volume area expressed as SW increased during exercise from 0.63 +/- 0.07 to 0.69 +/- 0.10 (P < 0.05). After adrenergic blockade, the Ees-to-Ea ratio was not significantly altered during exercise (0.90 +/- 0.24 vs. 0.83 +/- 0.15, P = NS). At rest and during exercise, both with intact reflexes and after beta-adrenergic blockade, the ratio of Ees to Ea remained within the range in which SW is > 95% of maximum. We conclude that during exercise, beta-adrenergic stimulation shifts the LV Pes-Ves relation to the left with an increased slope. This more than offsets the increase in Ea.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1993

Curvilinearity of LV end-systolic pressure-volume and dP/dtmax-end-diastolic volume relations.

We investigated the effect of contractile state (CS) on the curvilinearity of the left ventricular (LV) end-systolic pressure-volume (Pes-Ves) and the dP/dtmax-end-diastolic volume (dP/dtmax-Ved) relations in eight anesthetized open-chest dogs. LV volume was determined from three orthogonal diameters measured by sonomicrometry. The Pes-Ves relation and dP/dtmax-Ved relation were assessed during transient vena caval occlusion and aortic constriction, while CS was altered with dobutamine. At all CS, both relations were linear when volumes were decreased by caval occlusion. However, at higher volumes obtained by aortic constriction, the relations became nonlinear. At enhanced CS, the nonlinearity of both the Pes-Ves relation and the dP/dtmax-Ved relation increased. The dP/dtmax-Ved relation began to deviate from linearity at larger volumes, but closer to baseline operating volume, than the Pes-Ves relation. The relation between end-systolic mean circumference stress and wall strain (sigma es-epsilon es) was linear at control CS when the Pes-Ves relation was nonlinear but became nonlinear with enhanced CS. We conclude that both the Pes-Ves relation and the dP/dtmax-Ved relation are nonlinear, saturating at higher volumes. With increased CS, the nonlinearity of both relations increases. This CS-dependent curvilinearity of the Pes-Ves relation is due to both CS-dependent nonlinearity of the sigma es-epsilon es relation (consistent with length-dependent activation) and geometric factors that alter the relation between Pes and sigma es.

Animals↗
PubMed1993

Effect of heart failure on the mechanism of exercise-induced augmentation of mitral valve flow.

The exercise response of left ventricular (LV) filling dynamics may be altered by congestive heart failure (CHF). Accordingly, we studied 18 conscious dogs, instrumented to measure micromanometer LV and left atrial (LA) pressures and determine LV volume from three dimensions. CHF was produced by 4-5 weeks of right ventricular rapid pacing. Before CHF, exercise (5.5-8.5 mph for 8-15 minutes) increased the maximum rate of LV filling (dV/dtmax) (197 +/- 37 versus 297 +/- 56 ml/sec [mean +/- SD], p < 0.05) in response to an increase in the maximum early diastolic LA to LV pressure gradient (5.8 +/- 2.0 versus 9.8 +/- 1.9 mm Hg, p < 0.05) produced by a fall in minimum LV pressure (1.0 +/- 2.9 versus -3.9 +/- 3.1 mm Hg, p < 0.01), whereas mean LA pressure was unchanged (6.4 +/- 3.1 versus 6.4 +/- 4.2 mm Hg, p = NS). The time constant of LV relaxation was shortened (28.1 +/- 3.2 versus 21.0 +/- 4.2 msec, p < 0.05). After CHF, dV/dtmax (141 +/- 51 versus 200 +/- 59 ml/sec, p < 0.05) and the maximum LA to LV pressure gradient (6.0 +/- 1.1 versus 11.1 +/- 2.7 mm Hg, p < 0.05) continued to increase with exercise (3-5.0 mph for 4-8 minutes). However, the time constant of LV relaxation was prolonged (35.6 +/- 4.8 versus 38.9 +/- 5.5 msec, p < 0.05), and minimum LV pressure (15.1 +/- 5.6 versus 17.6 +/- 5.9 mm Hg, p < 0.05) and mean LA pressure increased (22.6 +/- 7.2 versus 29.1 +/- 7.3 mm Hg, p < 0.05). These altered effects of exercise on LV diastolic filling dynamics persisted when heart rate and wall stress during exercise before and after CHF were matched by varying the level of exercise. We conclude that, during normal exercise, mitral valve flow is augmented by a fall of early diastolic LV pressure without a rise in LA pressure. After CHF, early diastolic LV pressure does not fall but increases during exercise. Thus, the increase in the early diastolic LA to LV pressure gradient and the rate of mitral valve flow results from an increase in LA pressure during exercise after CHF. This study suggests that the failure of the enhancement of LV relaxation and an increase in early diastolic LV pressure with exercise after CHF may contribute to exercise intolerance in CHF.

Adrenergic beta-Antagonists↗
PubMed1992

Potential precipitating factors of the onset of myocardial infarction.

Myocardial infarction (MI) usually results from thrombotic coronary artery occlusion at the site of a ruptured atherosclerotic plaque. The factors responsible for triggering MI are not known but conditions that increase serum catecholamines may be involved. Accordingly, the authors prospectively evaluated the presence of factors that may increase catecholamines immediately prior to MI in 186 patients. Myocardial infarction was documented by a rise in serum CK-MB. There were 149 men and 37 women, aged 57 +/- 12 (mean +/- SD) years. All patients were interviewed within 72 hours of admission concerning strenuous physical activity, emotional stress, and assumption of the upright posture immediately prior to the onset of symptoms. Seventy-five (40%) patients had one or more of these factors immediately prior to the onset of MI chest pain. Fourteen (8%) experienced acute emotional upset; 28 (15%) were involved in strenuous physical activity; and 39 (21%) had suddenly changed position. In the latter group, 18 changed from being supine for more than 1 hour to standing; three rose from supine to sitting; and 18 changed from prolonged sitting (greater than 60 minutes) to standing. The conclusion is that a potential triggering factor is present in many patients immediately prior to the onset of MI. A sudden change in position is the most frequent potential trigger, typically occurring the morning after awakening from sleep.

Circadian Rhythm↗
PubMed1992

Restraining effect of intact pericardium during acute volume loading.

To determine the effect of the intact pericardium on ventricular end-diastolic pressures (EDP) during acute volume loading, we measured left ventricular (LV) and right ventricular (RV) micromanometer pressure and LV volume using a conductance catheter in eight open-chest, anesthetized dogs. A range of LV pressure and volume was obtained by intravascular volume expansion with the pericardium intact and then over a similar range after removal of the pericardium. Pericardial pressure (Pper) was calculated using static equilibrium analysis as the difference between LVEDP with the pericardium present and absent at a constant LV volume. At the beginning of the fluid infusion (LVEDP 7.3 +/- 1.7 mmHg and RVEDP 4.4 +/- 2.6 mmHg, mean +/- SD), Pper was not different from zero (-1.0 +/- 2.3 mmHg, P not significant). The onset of pericardial restraint (Pper greater than or equal to 0 mmHg) occurred when LVEDP was 9.1 +/- 2.9 mmHg and RVEDP was 4.1 +/- 2.9 mmHg. At low cardiac volumes before fluid infusion, RV transmural pressure was positive and significantly greater than the near zero Pper. After the onset of pericardial restraint, however, RVEDP and Pper increased similarly and were related according to Pper = 1.1 (+/- 0.34) RVEDP - 4.2 (+/- 2.6) mmHg, standard deviation 0.6 +/- 0.8 mmHg, r = 0.98 +/- 0.10. These data indicate that the intact pericardium behaves in two functionally distinct ways. At low cardiac volumes, Pper is zero and the pericardium does not affect LV filling. RV transmural pressure is positive and greater than Pper.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗