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Biomedical subjects

R M Lang

Publications and source records attributed to R M Lang.

At least 127 records · Page 7Linked to original sources

Effects of dopamine on left ventricular afterload and contractile state in heart failure: relation to the activation of beta 1-adrenoceptors and dopamine receptors.

Although long-term therapy with oral beta-adrenoceptor agonists in patients with heart failure is generally associated with the development of diminished pharmacologic efficacy, the ingestion of levodopa, which is decarboxylated endogenously to dopamine, is associated with a sustained improvement in cardiac function. The beneficial hemodynamic actions of dopamine in patients with heart failure have been attributed to a positive inotropic effect that is mediated through activation of beta 1-adrenoceptors. However, a reduction in left ventricular afterload resulting from the activation of dopamine receptors may also lead to an improvement in the performance of the failing heart. To ascertain the relative importance of the positive inotropic and afterload-reducing effects of dopamine in patients with heart failure, dopamine (2, 4, 6 micrograms/kg per min), dobutamine (2, 6, 10 micrograms/kg per min) and nitroprusside (0.125 to 2.0 micrograms/kg per min) were administered to 13 patients with dilated cardiomyopathy while monitoring left ventricular wall thickness and dimensions by echocardiography and left ventricular and aortic pressures with a micromanometer-tipped catheter. Altering left ventricular afterload, quantified as end-systolic circumferential wall stress, with nitroprusside allowed generation of the left ventricular end-systolic circumferential wall stress-velocity of fiber shortening relation that represented the baseline contractile state of the myocardium. Left ventricular velocity of fiber shortening was elevated during the administration of dobutamine and dopamine when compared with measurements obtained with nitroprusside at the same left ventricular end-systolic circumferential wall stress. Furthermore, left ventricular end-systolic wall stress decreased with dopamine but not with dobutamine. Thus, the beta 1-adrenoceptor activity of dopamine and dobutamine augmented the contractile state of the myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Physiologic mechanisms governing hemodynamic responses to positive inotropic therapy in patients with dilated cardiomyopathy.

Clinical trials in patients with dilated cardiomyopathy (DCM) have shown a wide disparity in the hemodynamic responses to positive inotropic therapy. In addition, the response of the failing left ventricle to positive inotropic agents reflects the net interaction of multiple factors, including the magnitude of contractile abnormality and compensatory mechanisms. In the current study, left ventricular geometry, loading conditions, and contractile state were assessed in 13 patients with nonischemic DCM with the use of simultaneous high-fidelity pressure measurements and echocardiographic recordings. Comparisons were made with echocardiographic and calibrated carotid pulse data acquired in nine age-matched normal subjects. The patients with DCM were divided according to the left ventricular end-diastolic wall thickness-to-dimension ratio into groups with "appropriate" hypertrophy (i.e., less than or equal to 2 SDs from mean normal; n = 5; group 1) and "inadequate" hypertrophy (i.e., greater than 2 SDs from mean normal; n = 8; group 2). Age, New York Heart Association functional class, left ventricular wall mass index, and left ventricular end-diastolic pressure and dimension were similar for the DCM groups. Baseline left ventricular afterload (defined as circumferential end-systolic wall stress, sigma es) was 168% and 203% greater than normal in groups 1 and 2, respectively. The administration of the beta-adrenoceptor agonist dobutamine decreased left ventricular afterload by 12% in the normal subjects and by 10% in group 1 patients, while augmenting afterload by 5% in group 2 patients. The latter response occurred despite a 17% fall in systemic vascular resistance. Overall left ventricular performance, as assessed by the rate-corrected mean velocity of fiber shortening (Vcfc), was related to left ventricular afterload (i.e., sigma es). The resultant sigma es -Vcfc relationship, a sensitive measure of left ventricular contractility, was determined over a wide range of afterload conditions generated by methoxamine (normal subjects) or nitroprusside (DCM). Baseline left ventricular contractile state was 61% of normal for group 1 and 44% of normal for group 2. The contractile response to dobutamine infusion was 52% of normal for group 1 and only 22% of normal for group 2. Thus, positive inotropic therapy with dobutamine in patients with DCM is limited by (1) an attenuated contractile response and (2) elevated left ventricular afterload, which may be augmented further during its administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiomyopathy, Dilated↗

Role of adrenoceptors and dopamine receptors in modulating left ventricular diastolic function.

Although both dopamine and dobutamine are potent positive inotropic agents, multiple studies indicate that dopamine may produce a rise in left ventricular (LV) filling pressure, while dobutamine often has the opposite effect. To ascertain the pharmacological and hemodynamic mechanisms responsible for the elevation in LV filling pressure observed with dopamine, we administered incremental infusions (2, 4, and 6 micrograms/kg/min) of dopamine to 18 open-chest, anesthetized dogs in the presence and absence of rauwolscine (selective alpha 2-adrenoceptor antagonist) (n = 7), terazosin (selective alpha 1-antagonist) (n = 6), and domperidone (selective dopamine2 antagonist) (n = 5), while measuring pressures in the LV and left atrium and changes in dimension in the LV short-axis (with ultrasonic piezo crystals). Dobutamine (2, 4, and 6 micrograms/kg/min) was infused in five additional dogs before and after administration of rauwolscine. The time constant of isovolumic pressure decay, peak lengthening rate (mm/sec), LV end-diastolic pressure, and diastolic pressure-dimension relation were computed. A significant elevation in LV end-diastolic pressure and a parallel increase in LV end-diastolic chamber size was observed with dopamine, while a decline in LV end-diastolic pressure occurred with dobutamine. Yet both dopamine and dobutamine caused a dose-related acceleration of pressure decay and augmentation of peak lengthening rate. Furthermore, heart rate declined during the administration of dopamine but rose with dobutamine. In the presence of either rauwolscine or terazosin, dopamine infusion resulted in a positive chronotropic effect and dose-dependent reductions in LV end-diastolic pressure and end-diastolic chamber dimension; arterial pressure fell only after terazosin administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Left ventricular contractility varies directly with blood ionized calcium.

STUDY OBJECTIVE: To determine the effect of variations in blood ionized calcium (Ca2+) on myocardial contractility independent of changes in loading conditions and other biochemical variables. DESIGN: Hemodialysis done in a randomized, double-blind manner with dialysates differing in calcium concentration only. Left ventricular contractility was assessed using the load- and heart rate-independent relationship between end-systolic wall stress (sigma es) and rate-corrected velocity of fiber shortening (Vcfc). SETTING: In-hospital dialysis unit and echocardiography laboratory of a university medical center. PATIENTS: Seven patients with stable, chronic renal failure maintained on regular hemodialysis. INTERVENTIONS: Each patient was hemodialyzed three times within 1 week with dialysates differing in calcium concentration only. Ultrafiltration was adjusted to achieve the same postdialysis weight. Immediately after dialysis, two-dimensionally targeted M-mode echocardiographic and calibrated carotid pulse tracings were recorded over a wide range of left ventricular end-systolic wall stress values (a measure of left ventricular afterload) generated by either methoxamine or nitroprusside. MEASUREMENTS AND MAIN RESULTS: After dialysis, three statistically distinct levels of Ca2+ were achieved. When Ca2+ was 1.34 +/- 0.03 mmol/L, Vcfc, calculated at a common level of afterload (sigma es = 50 g/cm2), was 1.01 +/- 0.05 cir/sec; at low Ca2+ (1.02 +/- 0.02 mmol/L), Vcfc fell to 0.89 +/- 0.04 cir/sec (P less than 0.001 compared with medium); at high Ca2+ (1.68 +/- 0.07 mmol/L) Vcfc rose to 1.10 +/- 0.03 circ/sec (P less than 0.001 compared with medium and low). CONCLUSION: Variations in Ca2+ are directly correlated with clinically significant changes in myocardial contractility.

Adult↗

Effect of intracoronary injections of sonicated microbubbles on left ventricular contractility.

Despite the recent interest in contrast-enhanced echocardiography as a means of defining myocardial perfusion, the effects of echo contrast agents on left ventricular (LV) contractility in humans remains poorly defined. This is particularly relevant because intracoronary injection of contrast agents used for angiographic visualization of coronary arteries produces significant alterations in LV hemodynamics. The relation of LV end-systolic wall stress (sigma es) to rate-corrected velocity of fiber shortening (Vcfc), a load-independent index of contractility, was studied in 7 patients undergoing elective coronary arteriography. Two-dimensional and targeted M-mode echocardiographic and central aortic pressure tracings were recorded during injections of standard volumes of angiographic (7 to 9 ml of nonsonicated Renografin-76) and echocardiographic (1.5 to 2.0 ml of sonicated Renografin-76) contrast agents into the left main coronary artery. The order in which agents were injected was randomly determined. Myocardial contractility was assessed under control conditions and 5 and 15 seconds after injection. Alterations in contractility relative to control were measured as the change in Vcfc after elimination of afterload (sigma es) as a confounding variable. An injection of Renografin-76 adequate for angiographic imaging of coronary artery anatomy resulted in a significant depression of LV contractility (p less than 0.001) in conjunction with a tendency toward increased afterload (p = 0.12); recovery occurred by 15 seconds after injection. The smaller amounts of sonicated Renografin-76 required to give adequate contrast enhancement of the myocardium did not alter LV contractile state or afterload.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Echocardiographic contrast agents: effect of microbubbles and carrier solutions on left ventricular contractility.

Recently, there has been a resurgence of interest in the use of contrast-enhanced echocardiography as a means of noninvasively assessing myocardial perfusion. However, if injections of echocardiographic contrast agents are to be used for this purpose it is essential that they are not intrinsically toxic to the heart. In this study, the left ventricular end-systolic wall stress-rate-corrected velocity of fiber shortening relation, a load independent index of contractility, was studied in nine dogs. Two-dimensional and targeted M-mode echocardiographic as well as central aortic pressure tracings were made during echocardiographically gated, pressure- and volume-controlled aortic root injections of nonsonicated and sonicated Renografin-76, saline and dextrose 70% (n = 6), and sonicated and hand-agitated Renografin-76/saline mixture (n = 5). Two of nine dogs received all agents. Off-line computer videodensitometric analysis documented myocardial perfusion. In all cases, data were obtained at control and 5 and 15 seconds after injection. Additional data were collected at 25 seconds after injection for the Renografin-76/saline mixture. Alterations in contractility were measured relative to control as changes in rate-corrected velocity of fiber shortening after afterload (measured as end-systolic wall stress) was eliminated as a confounding variable. Under no condition did saline or Renografin-76 cause alterations in left ventricular contractility. Nonsonicated and sonicated dextrose 70% increased left ventricular contractility at 15 seconds but not at 5 seconds after injection. Hand-agitated Renografin-76/saline mixture induced a negative inotropic effect at 5 and 15 seconds after injection.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Contrast ultrasonography of the kidney: a new method for evaluation of renal perfusion in vivo.

Assessment of the effects of pharmacologic agents on renal blood flow (RBF) is clinically important in many disease states, including hypertension and congestive heart failure. However, because of the complexities of RBF, quantitation in vivo has been technically difficult. This study demonstrates the utility of ultrasound imaging of the kidney combined with injection of a sonicated radiocontrast solution (Renografin-76) for the assessment of regional renal blood flow. The technique uses a suspension of uniform microbubbles (diameter 4.4 +/- 2.8 micron), which when injected directly into the descending aorta are distinctly visualized by renal ultrasound. Five dogs were studied. Catheters were placed in the descending aorta for injection of sonicated Renografin and in the renal artery for drug infusions. Data were collected before and during intrarenal artery infusions of bradykinin and norepinephrine. Total RBF was measured by electromagnetic flowmeter. Video density time curves were generated for comparable segments of the outer renal cortex and fit to a monoexponential decay curve. This allowed calculation of the mean exponential decay index (t1/2). An increase in t1/2 paralleled decreased renal perfusion (i.e., longer washout of contrast material). The opposite was true for a decrease in t1/2. Bradykinin increased RBF from 134 +/- 26 to 249 +/- 19 ml/min (p less than .01 vs control), and norepinephrine decreased RBF from 130 +/- 25 to 51 +/- 17 ml/min (p less than .01 vs control).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Contrast echocardiography for evaluation of myocardial perfusion: effects of coronary angioplasty.

Assessment of viable myocardium before and after interventional therapy has become a critical issue in modern cardiology. This report describes a new contrast echocardiographic technique using conventional two-dimensional imaging during direct intracoronary injections of small volumes (1.5 to 2.0 cc) of sonicated Renografin-76. Contrast echocardiography was performed before and after coronary angioplasty in seven patients with single vessel coronary artery disease. Before angioplasty a contrast (that is, perfusion) defect was noted in all seven patients. This defect correlated with the anatomic distribution of the epicardial coronary stenosis. After angioplasty the mean gradient across the stenotic lesion decreased from 52 +/- 11 to 13 +/- 14 mm Hg (p less than 0.01) in association with a fall in the mean diameter of the lesion from 84 +/- 8 to 29 +/- 13% (p less than 0.001). Increased myocardial perfusion to the area of "contrast defect" was demonstrated in only five of the seven patients, despite hemodynamically and angiographically successful angioplasty. Thus, contrast echocardiographic techniques performed during interventional therapy and used in conjunction with standard coronary angiographic procedures may provide additional physiologic information regarding regional myocardial perfusion after attempts at revascularization.

Aged↗

Myocardial mechanics in hyperthyroidism: importance of left ventricular loading conditions, heart rate and contractile state.

Hyperthyroidism has been reported to affect all of the major determinants of left ventricular performance in a manner that would augment ventricular shortening characteristics. The hypothesis tested in this study is that reduced afterload in conjunction with increased preload and heart rate, rather than augmented contractility, accounts for much of the increase in left ventricular performance noted previously in these patients. To investigate this hypothesis, 11 hyperthyroid patients were evaluated serially over 4 +/- 2 months. With therapy, serum total thyroxin (T4) decreased significantly (p less than 0.001). Ventricular hemodynamics were assessed by two-dimensional targeted M-mode echocardiograms and calibrated carotid pulse tracings. Ventricular preload was estimated by end-diastolic dimension, whereas afterload was measured as end-systolic wall stress. Overall left ventricular performance was quantitated by the extent and velocity of shortening, whereas myocardial work was assessed by ventricular systolic stress-length relations. With therapy, overall left ventricular performance declined (p less than 0.01). This change was associated with no change in end-diastolic dimension or end-systolic wall stress, and a 24% fall in heart rate (p less than 0.01). This latter finding has been shown previously to have no significant effect on left ventricular contractile state over the range of heart rates encountered in this study. In all cases, the end-systolic stress/rate-corrected shortening velocity relation fell with attainment of normal thyroid status, characteristic of a decline in contractility. There was a strong positive correlation between left ventricular contractility and serum thyroid hormone level (r = 0.83). In addition, ventricular minute work declined with therapy (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Effects of acute lung injury and anesthesia on left ventricular mechanics.

Traditional left ventricular (LV) function curves are frequently depressed in patients with acute lung injury. Similar findings in pentobarbital sodium-anesthetized dogs with oleic acid lung injury (OALI) have been observed. To test the hypothesis that acute OALI produces a significant injury to the heart, the LV mechanics of pentobarbital-anesthetized dogs with (n = 6) and without (n = 6) OALI were evaluated. End-systolic force-length and force-velocity relations determined echocardiographically during afterload manipulation with sodium nitroprusside demonstrated a marked deterioration in LV shortening characteristics over 90 min in both groups of pentobarbital-anesthetized dogs. In contrast, LV mechanics studied using the same protocol in fentanyl-anesthetized dogs were unchanged in both the injured (n = 6) and noninjured (n = 6) lung groups. Comparisons with data acquired over a wide range of LV afterload from six conscious, instrumented dogs showed that LV contractile state was normal to slightly increased with fentanyl and markedly depressed with pentobarbital. Diastolic properties, as assessed by end-diastolic pressure-dimension relations, were essentially unchanged in all anesthetized animals. We conclude that OALI has no effect on LV systolic or diastolic mechanics; the LV dysfunction attributed to OALI in previous studies is due to an acute, severe cardiomyopathy induced by pentobarbital; and unlike pentobarbital, anesthesia with fentanyl has no discernible time-dependent effect on LV mechanics. These findings have important implications for future studies of canine cardiovascular physiology employing anesthetized animal preparations.

Anesthesia↗

The differential effects of positive inotropic and vasodilator therapy on diastolic properties in patients with congestive cardiomyopathy.

Symptoms of congestive heart failure frequently reflect abnormalities in both systolic and diastolic performance. While much work has been reported regarding the mechanisms by which positive inotropic and vasodilator therapy affect systolic performance, little is known about their effect on diastolic function. In 12 patients with diffuse congestive cardiomyopathy micromanometer left ventricular and aortic pressure measurements were recorded simultaneously with two-dimensionally targeted M mode echocardiograms and thermodilution-determined cardiac output. Each patient received dopamine (2, 4, and 6 micrograms/kg/min), and dobutamine (2, 6, and 10 micrograms/kg/min), and 10 received nitroprusside (0.125 to 2.0 micrograms/kg/min). Baseline hemodynamics were characterized by low cardiac index (2.1 +/- 0.7 liter/min/m2, mean +/- SD), high left ventricular end-diastolic pressure (24 +/- 10 mm Hg), and increased end-diastolic (6.8 +/- 1.0 cm) and end-systolic dimensions (6.0 +/- 1.0 cm). All patients had abnormal left ventricular pressure decay with a prolonged time constant (67 +/- 20 msec) and reduced peak diastolic lengthening rates. Dopamine and dobutamine decreased the time constant of relaxation and increased the peak lengthening rate. Dobutamine also reduced the minimum diastolic pressure from 14 +/- 7 to 10 +/- 9 mm Hg (p less than .01); neither drug reduced end-diastolic pressure. In fact, dopamine elevated end-diastolic pressures in seven patients, despite more rapid pressure decay. Diastolic pressure-dimension relations after dopamine and dobutamine showed a leftward shift with a reduced end-systolic chamber size, but no significant changes in passive chamber stiffness. Nitroprusside decreased left ventricular minimum diastolic pressure by 4 +/- 2 mm Hg and end-diastolic pressure by 7 +/- 4 mm Hg (p less than .01). It did not consistently accelerate left ventricular pressure decay at the doses tested. The decreased end-diastolic pressure with nitroprusside was due to a reduced end-diastolic dimension in five patients. In the other patients, all of whom had elevated right atrial pressures, diastolic pressure-dimension relations showed a parallel downward shift after nitroprusside. Thus, positive inotropic therapy with beta 1-adrenoceptor agonists enhances early diastolic distensibility by accelerating relaxation, augmenting filling, and reducing end-systolic chamber size. Vasodilator therapy is much more effective in lowering diastolic pressures.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

Systemic vascular resistance: an unreliable index of left ventricular afterload.

Systemic vascular resistance (SVR) is a frequently used clinical index of left ventricular afterload. However, SVR may not adequately assess left ventricular afterload (i.e., ventricular internal fiber load during systole) since it reflects only peripheral vasomotor tone. In contrast, left ventricular end-systolic wall stress (sigma es) reflects the combined effects of peripheral loading conditions and left ventricular chamber pressure, dimension, and wall thickness. To determine the relationship between SVR and sigma es, left ventricular afterload and contractility were pharmacologically altered in eight dogs instrumented with central aortic microtip and Swan-Ganz thermodilution catheters. Left ventricular wall thicknesses and dimensions were measured from two-dimensionally targeted M mode echocardiograms. Aortic, right atrial, and left ventricular end-systolic pressures as well as cardiac output were recorded. SVR and sigma es were determined under control conditions as well as during infusions of nitroprusside, methoxamine, dobutamine, and norepinephrine. Control data acquired before each drug infusion were similar. When compared with baseline values, SVR underestimated the magnitude of change in left ventricular sigma es by 22% when afterload alone was decreased (nitroprusside), 54% when afterload alone was increased (methoxamine), and 50% when afterload was decreased and contractility was augmented (dobutamine). Most importantly, when afterload was minimally decreased in association with augmented contractility (norepinephrine), SVR increased by 21% while sigma es fell by 9%. Thus, discordant changes in left ventricular afterload (i.e., sigma es) and SVR can occur during pharmacologic interventions. SVR is an unreliable index of left ventricular afterload, reflecting only peripheral arteriolar tone rather than left ventricular systolic wall force. This emphasizes the fact that a true measure of left ventricular afterload must consider the interaction of factors internal and external to the myocardium.

Animals↗

Milrinone versus dobutamine: contribution of altered myocardial mechanics and augmented inotropic state to improved left ventricular performance.

Milrinone and dobutamine are positive inotropic agents with complex mechanisms of action. Traditional indexes of left ventricular function are unable to determine how much of the improvement in cardiac performance induced by these drugs is due to augmented inotropy and how much is the result of afterload reduction. Recently, the end-systolic wall stress (sigma es)-rate corrected velocity of fiber shortening (Vcfc) relationship has been shown to be a sensitive measure of contractility that is independent of preload while incorporating afterload. This index was measured in two groups of normal subjects (n = 8 per group) over a wide range of aortic pressures generated by administration of methoxamine before and during (1) milrinone or (2) dobutamine infusion. Studies were performed with the use of echocardiographic and calibrated carotid pulse tracings. Milrinone and dobutamine produced similar increases in overall left ventricular performance. Milrinone decrease end-systolic dimension (Des) by 15% and end-systolic pressure (Pes) by 22%, while increasing end-systolic wall thickness (hes) by 14%. This resulted in a 43% decline in left ventricular afterload as measured by sigma es. In contrast, dobutamine decreased Des by 11% while increasing hes by 14% and Pes by 22%. Despite the increase in left ventricular pressure, sigma es fell by 20%. Since afterload reduction alone results in increased left ventricular shortening, analysis of left ventricular performance was performed for both drugs at matched levels of sigma es under control and positive inotropic conditions. Twenty-nine percent of the improvement in Vcfc produced by milrinone was due to a decrease in afterload as compared with 18% of that produced by dobutamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Relation of electrocardiographic R-wave amplitude to changes in left ventricular chamber size and position in normal subjects.

Although exercise-induced changes in electrocardiographic R-wave amplitude have been ascribed to changes in left ventricular (LV) size, QRS axis, heart rate and ischemia, the physiologic mechanism remains unclear. To clarify the relation between R-wave amplitude and changes in LV size and position, simultaneous 9-lead electrocardiograms and targeted M-mode echocardiograms were recorded from 15 normal subjects. Recordings were made at rest, during Valsalva maneuver and during methoxamine infusion. LV diastolic dimension increased with methoxamine and decreased with Valsalva maneuver (p less than 0.001). R-wave amplitude in leads V5 and V6 varied directly with LV dimensions (p less than 0.001). The correlation coefficient between the change in R-wave amplitude in V5 or V6 and the change in LV dimension was 0.81 (p less than 0.01). No significant changes in R-wave amplitude were seen in electrocardiographic leads I, II, III, aVR, aVL, aVF or V1. Distance from the chest wall to the LV posterior wall correlated with change in R-wave amplitude (r = 0.79, p less than 0.001). Change from supine to left lateral position moved the left ventricle closer to the lateral chest wall in association with a 41 +/- 8% increase in R-wave amplitude in V5 and V6 (p less than 0.001). In conclusion, there is a direct and a dynamic relation between R-wave amplitude and LV chamber size. Chamber size and distance from the left ventricle to leads V5 or V6 interact as major determinants of R-wave amplitude.

Adult↗

Change in ventricular cavity size: differential effects on QRS and T wave amplitude.

Although many factors have been reported to change the R wave amplitude of the electrocardiogram (ECG), few observations have been made of the associated changes in T wave amplitude. We hypothesized that changes in R and T wave amplitude should parallel each other. To test this hypothesis, R and T wave amplitudes were measured in 15 normal subjects during increased and decreased left ventricular dimensions induced by infusion of methoxamine and by Valsalva maneuver, respectively, as well as during changes in the proximity of the left ventricle to the chest wall (i.e., shift in patient position from supine to left lateral position). Simultaneous nine-lead ECGs and two-dimensional-guided M mode echocardiograms of the left ventricle were recorded at rest and under each experimental condition. R wave amplitude increased as the left ventricular lateral wall moved closer to the V5 and V6 electrodes. Alterations in R wave amplitude seen with changes in left ventricular chamber size were primarily caused by radial movement of the left ventricle in relation to the chest wall. Proximity of the left ventricle to the chest wall was therefore a major determinant of R wave amplitude. In contrast, T wave amplitude varied directly with alterations in left ventricular chamber size but was unaffected by changes in proximity to the recording electrode on the chest wall. Left ventricular chamber size, and possibly the associated alteration in endocardial-to-epicardial surface area ratio, appeared to be the major determinants of T wave amplitude.

Adult↗

Adverse cardiac effects of acute alcohol ingestion in young adults.

Previous studies of the effects of acute alcohol ingestion in normal subjects have used measures of left ventricular performance that are altered by changes in preload and afterload and in contractile state. In studies involving nine healthy, young adults, we measured sensitive load-independent end-systolic indices of left ventricular contractility over a wide range of pressures generated by methoxamine infusion before and after oral alcohol administration. Echocardiography was used in conjunction with calibrated carotid pulse tracings. Alcohol ingestion resulted in a fall (p less than 0.01) in left ventricular end-diastolic dimension (a measure of preload), end-systolic wall stress (a measure of afterload), and systemic vascular resistance, while not changing the left ventricular shortening fraction. In contrast, the end-systolic pressure-dimension slope decreased (p less than 0.001) and the rate-corrected velocity of left ventricular fiber shortening at an end-systolic wall stress of 50 g/cm2 fell (p less than 0.001). Thus, when load-independent assessment of left ventricular contractility is done, acute alcohol ingestion has a myocardial depressant effect greater than previously suspected.

Adult↗

Pregnancy and heart disease.

The maternal cardiovascular system undergoes extensive changes during pregnancy. These changes become especially important in women with underlying cardiac disease. In order to provide a basis for understanding cardiac disease in pregnancy, the authors provide a discussion of the normal cardiovascular physiology of pregnancy, followed by a review of the types of heart disease in women of childbearing age.

Adrenergic beta-Antagonists↗