Biomedical subjects

R V Ditchey

Publications and source records attributed to R V Ditchey.

At least 19 recordsLinked to original sources

PubMed1994

Phenylephrine plus propranolol improves the balance between myocardial oxygen supply and demand during experimental cardiopulmonary resuscitation.

Epinephrine increases coronary blood flow but may not improve the balance between myocardial oxygen supply and demand during cardiopulmonary resuscitation (CPR). The objective of this study was to determine whether this balance can be improved by administering a relatively pure alpha-adrenergic vasoconstrictor, alone or in combination with a beta-adrenergic blocker. We measured coronary perfusion pressures during CPR and myocardial adenosine 5'-triphosphate (ATP) and lactate concentrations in biopsies obtained immediately after 10 minutes of CPR in six control dogs and in three groups of six dogs each given large doses of epinephrine, phenylephrine, or phenylephrine plus propranolol during CPR. Coronary perfusion pressure during CPR was higher in the three treated groups than in the control group, although differences were limited to the early portion of CPR in dogs given epinephrine or phenylephrine alone. Postresuscitation myocardial ATP concentration was significantly higher (29.5 +/- 3.0 vs 22.6 +/- 1.8 nmol/mg of protein, p < 0.05) and myocardial lactate concentration tended to be lower (52.8 +/- 13.6 vs 78.5 +/- 15.2 nmol/mg of protein) than in the control group in dogs given both phenylephrine and propranolol. In contrast, myocardial ATP concentration tended to be lower than in the control group in epinephrine-treated dogs, and myocardial lactate concentrations were higher than in the control group in dogs treated with either epinephrine (p < 0.05) or phenylephrine alone (p = 0.052). We conclude that the balance between myocardial oxygen supply and demand during CPR can be improved by administering a combination of phenylephrine and propranolol, but not by administering large doses of epinephrine or phenylephrine alone.

Adenosine Triphosphate↗

PubMed1994

Beta-adrenergic blockade reduces myocardial injury during experimental cardiopulmonary resuscitation.

OBJECTIVES: We attempted to determine the effects of beta-adrenergic blockade during cardiopulmonary resuscitation (CPR) on defibrillation rates and postresuscitation left ventricular function. BACKGROUND: The results of previous studies suggest that propranolol administration can both reduce myocardial oxygen requirements and increase coronary perfusion pressure during CPR. METHODS: Left ventricular pressure and segment length were measured before and after 5 min of CPR in 22 dogs either given epinephrine (0.015 mg/kg body weight at the onset and after 4 min) or pretreated with propranolol (2 mg/kg) and given epinephrine during CPR. RESULTS: Despite identical epinephrine doses, coronary perfusion pressure during CPR was higher in the epinephrine plus propranolol group (p < 0.05), and defibrillation was successful in 9 of 11 dogs given both epinephrine and propranolol versus 6 of 11 dogs given epinephrine alone (p = NS). Peak and developed left ventricular pressures, left ventricular end-diastolic pressure and the peak rate of left ventricular pressure development (+dP/dt) did not differ between study groups when measured either 5 or 15 min after successful defibrillation. However, when survivors in the epinephrine group were given propranolol after CPR to eliminate compensatory sympathetic stimulation, left ventricular developed pressure and peak +dP/dt were lower (p < 0.05) despite trends toward higher left ventricular end-diastolic pressures and normalized end-diastolic segment lengths compared with dogs given propranolol before CPR. CONCLUSIONS: These findings suggest that beta-adrenergic blockade reduces myocardial injury during CPR without decreasing the likelihood of successful defibrillation or compromising spontaneous postresuscitation left ventricular function.

Animals↗

PubMed1992

Myocardial oxygen requirements during experimental cardiopulmonary resuscitation.

OBJECTIVE: The aims were to determine myocardial oxygen requirements during cardiopulmonary resuscitation (CPR), and to test the hypothesis that endogenous catecholamines have a major effect on myocardial oxygen requirements in this setting. METHODS: Myocardial oxygen consumption (MVO2) was measured during 20 minutes of CPR in eight anaesthetised dogs. Coronary blood flow was maintained at prearrest levels using an external pump to provide a permissive level of oxygen delivery during ventricular fibrillation. Oxygen content was measured in arterial and coronary sinus blood samples under prearrest conditions and at 5 min intervals during CPR. Four dogs were given propranolol (1 mg.kg-1) following the 5 min measurements. RESULTS: MVO2 averaged 108.7(SEM 12.8)% of the initial prearrest values after 5 min CPR (n = 8). After 10 min CPR, MVO2 fell to 53.8(13.3)% of the initial prearrest values in the subset of animals given propranolol after the 5 min measurements (n = 4), but remained at prearrest levels in untreated animals (p < 0.05 for an interactive effect between treatment and time). MVO2 subsequently tended to decrease with time in untreated animals, but remained a high percentage of prearrest values throughout the 20 min period of CPR. CONCLUSIONS: These findings suggest that endogenous sympathetic stimulation of the fibrillating heart results in high myocardial oxygen requirements during CPR.

Animals↗

PubMed1988

Determinants of the relation between systolic pressure and duration of isovolumic relaxation in the right ventricle.

Previous studies have suggested that right ventricular systolic pressure can be predicted from noninvasive estimates of the interval between pulmonary valve closure and tricuspid valve opening. To determine the basis for this relation, phonocardiograms and high fidelity right atrial and ventricular pressures were recorded in 29 patients with a right ventricular systolic pressure ranging from 20 to 149 mm Hg. In 22 patients with normal right atrial pressure (less than or equal to 8 mm Hg), both the time interval and the magnitude of pressure decrease from pulmonary valve closure to tricuspid valve opening were linearly related to systolic pressure (r = 0.89 and 0.96, respectively). Early pulmonary valve closure (decreased "hang-out" time) contributed to the greater magnitude of isovolumic pressure decrease at high systolic pressures, but correction for hang-out time did not eliminate the relation between systolic pressure and the pulmonary valve closure-tricuspid valve opening interval (n = 10). When patients with documented right coronary artery disease were excluded, the time constant for isovolumic pressure decrease also increased as a function of systolic pressure (r = 0.67, p less than 0.01, n = 24), suggesting impaired relaxation at high systolic pressures. However, the mean rate of pressure decrease (mean negative dP/dt) still was greater in patients with a high pressure because of the exponential nature of the isovolumic pressure-time relation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1988

Human right ventricular end-systolic pressure-volume relation defined by maximal elastance.

This study was undertaken to determine 1) whether a combined radionuclide-hemodynamic technique could define the right ventricular end-systolic pressure-volume relation (RV ESPVR) in the clinical setting, 2) whether the human RV ESPVR defined by maximal elastance is linear and responsive to inotropic interventions, and 3) whether more easily measured modifications of the ESPVR are reliable substitutes as an index of RV function. Eight patients with normal RV function were studied with simultaneous micromanometer RV pressure measurements and radionuclide ventriculography to construct RV pressure-volume loops. Data were collected at baseline and after at least two alterations in loading conditions with nitroglycerin, phenylephrine, or saline. End systole was defined by maximal elastance (E(t) = P(t)/[V(t) - V0]). Data were also obtained during administration of dobutamine in four patients and after atrial pacing tachycardia in one patient. The RV ESPVR defined by maximal elastance was highly linear (r = 0.988-0.999) throughout the range of pressures and volumes tested. Furthermore, the linear correlations were significantly higher (p less than 0.005), and the linear regression standard error of the estimate (SEE) was significantly lower (p less than 0.005) for the RV ESPVR defined by maximal elastance compared with modifications of the ESPVR with the ratio of pulmonary artery-dicrotic notch pressure or RV peak pressure to end-ejection volume. Dobutamine or atrial pacing tachycardia produced a leftward shift of the entire RV pressure-volume loop, and in each patient (five of five), the point of maximal elastance fell outside the 95% confidence interval defined by the baseline ESPVR. However, because of the larger SEE, the leftward shift with modifications of the ESPVR was not statistically significant in any patient by the pulmonary artery-dicrotic notch pressure: end-ejection volume ratio and was significant in only one of five patients by the RV peak pressure: end-ejection volume ratio (p less than 0.03). Therefore, it appears that the steady-state RV ESPVR defined by maximal elastance in patients with normal RV function is responsive to alterations in inotropic state and is more sensitive to alterations in RV function than the frequently used, more easily measured modifications of the RV ESPVR.

Blood Pressure↗

PubMed1988

Failure of epinephrine to improve the balance between myocardial oxygen supply and demand during closed-chest resuscitation in dogs.

Although large doses of epinephrine increase coronary perfusion pressure and flow during cardiopulmonary resuscitation, epinephrine also increases myocardial oxygen consumption during ventricular fibrillation. To test the hypothesis that epinephrine improves the balance between myocardial oxygen supply and demand during cardiopulmonary resuscitation, myocardial adenosine 5'-triphosphate (ATP) and lactate concentrations were measured before and immediately after 10 minutes of cardiopulmonary resuscitation in 10 control dogs and 10 dogs given intravenous epinephrine (1-mg bolus followed by 0.2 mg/min). Left ventricular myocardial blood flow during cardiopulmonary resuscitation was measured with radioactive microspheres and was significantly higher in the epinephrine group (48 +/- 11 vs. 21 +/- 4 ml/min/100 g, p less than 0.05). However, myocardial lactate concentration increased significantly (p less than 0.01) after cardiopulmonary resuscitation in both groups and tended to increase more in epinephrine-treated animals. Myocardial ATP concentration decreased significantly (p less than 0.05) and by comparable amounts in the two groups. These findings suggest that large doses of epinephrine may fail to improve the balance between myocardial oxygen supply and demand during cardiopulmonary resuscitation, even when they result in a substantial increase in coronary blood flow.

Adenosine Triphosphate↗

PubMed1987

Right heart pressure does not equal pericardial pressure in the potassium chloride-arrested canine heart in situ.

Recently proposed concepts of pericardial surface pressure, as opposed to liquid pressure, have advanced our understanding of the relationship between pericardial and heart chamber pressures. However, the subsequent suggestion that right heart intracavitary pressure equals, or nearly equals, pericardial surface pressure is not strictly consistent with the physiology of pericardial constraint. If right heart pressure equals pericardial surface pressure, then transmural right heart pressure equals zero. Because of the difficulty in measuring pericardial pressure directly in the beating heart we designed an experiment in the recently arrested canine heart in situ to measure pericardial pressure indirectly and to test the hypothesis that right heart transmural pressure is zero under reasonably physiologic, static equilibrium conditions. According to a static equilibrium analysis of the pressures acting across the walls of the heart, at a given volume the change in right heart pressure caused by removing the pericardium is equal to the pericardial pressure when the pericardium is intact. We found that this drop in pressure caused by pericardiectomy did not equal right heart pressure and therefore that right heart transmural pressure does not equal zero.

Animals↗

PubMed1985

Metabolic evidence of inadequate coronary blood flow during closed-chest resuscitation in dogs.

Closed-chest cardiopulmonary resuscitation (CPR) produces only small pressure differences across the coronary circulation and relatively little coronary blood flow in dogs with ventricular fibrillation. To determine whether coronary flow during experimental resuscitation is sufficient to maintain aerobic myocardial metabolism, we measured left ventricular adenosine triphosphate (ATP) and lactate concentrations before and immediately after a 20 min period of CPR in six fibrillating dogs. The mean aortic-right atrial pressure difference generated during CPR averaged 5.4 +/- 2.6 mmHg (SEM) and 3.2 +/- 2.6 mmHg at the beginning and end of the 20 min period, respectively. Left ventricular myocardial blood flow (measured with radioactive microspheres) averaged 16.7 +/- 5.7% of prearrest values during the first 10 min of CPR, and 8.5 +/- 4.8% of prearrest values during the second 10 min of CPR. Biopsies after CPR contained less ATP (3.3 +/- 0.1 vs 4.7 +/- 0.5 nmol.mg-1, p less than 0.05) and more than seven times more lactate (14.7 +/- 3.1 vs 1.9 +/- 0.2 nmol.mg-1, p less than 0.01) than control biopsies. We conclude that coronary blood flow during CPR is inadequate relative to myocardial oxygen demands during ventricular fibrillation in dogs. The techniques developed in this study provide a potential means of assessing the effects of experimental interventions on myocardial oxygenation during CPR.

Adenosine Triphosphate↗

PubMed1985

A potential method of correcting intracavitary left ventricular filling pressures for the effects of positive end-expiratory airway pressure.

Based on the observation that positive end-expiratory airway pressure (PEEP) causes comparable increments in intrapericardial and right-sided intracardiac pressures, we hypothesized that intracavitary left ventricular filling pressures measured in the presence of PEEP can be corrected for increased intrathoracic pressure by subtracting the effects of PEEP on intracavitary right ventricular filling pressures. Ventricular function curves (aortic blood flow vs intracavitary left ventricular end-diastolic pressure [LVEDP]) were generated with and without 15 cm of water of PEEP in eight dogs. All curves were shifted to the right by PEEP (i.e., intracavitary LVEDP was higher for any submaximal level of aortic blood flow). However, when pressures measured in the presence of PEEP were "corrected" by subtracting the corresponding increment in intracavitary right ventricular end-diastolic pressure caused by PEEP at each level of ventricular filling, control and corrected PEEP data points appeared to fall on the same curve in five dogs, and differed only slightly in three dogs. Mean control and corrected PEEP curves derived by averaging polynomial regression coefficients for each condition differed significantly from uncorrected PEEP curves (p less than .05), but not from each other. Analogous curves based on mean left atrial pressure were corrected equally well by subtracting the effects of PEEP on mean right atrial pressure. We conclude that the increments in intracavitary right heart filling pressures caused by PEEP can be used to correct intracavitary left heart filling pressures for the effects of PEEP on intrathoracic pressure.

Animals↗

PubMed1984

Acute effects of doxorubicin (adriamycin) on left ventricular function in dogs.

Although chronic doxorubicin (adriamycin) cardiotoxicity often is attributed to repeated episodes of acute myocardial injury, the acute effects of doxorubicin on in vivo left ventricular performance have not been studied in a carefully controlled setting. Accordingly, we recorded high-fidelity left ventricular pressures and segmental dimensions before and after either intravenous or intracoronary doxorubicin in twelve open-chest dogs. Propranolol was administered to prevent reflex sympathetic stimulation, and heart rate was held constant by atrial pacing. Intravenous doxorubicin (1.5 mg/kg) (n = 6) caused significant decreases in all measured indices of myocardial contractility, in association with a large decrease in left ventricular systolic pressure (125 +/- 28 and 81 +/- 23 mm Hg before and 5 min after doxorubicin, respectively, P less than 0.01). Intracoronary doxorubicin (0.075 to 0.3 mg/kg) (n = 6) caused similar decreases in percent segment shortening (from 19 +/- 7 to 16 +/- 8, P less than 0.05), mean normalized shortening rate (from 0.87 +/- 0.34 to 0.71 +/- 0.37 segment lengths/sec, P less than 0.05), and peak positive left ventricular dP/dt (by 10 +/- 11%, P less than 0.07), although left ventricular systolic pressure was only modestly decreased (126 +/- 20 and 113 +/- 17 mm Hg before and after doxorubicin, respectively, P less than 0.01). Intracoronary doxorubicin also slowed the rate of left ventricular relaxation, as evidenced by an increase in the time constant for isovolumic pressure fall from 32.0 +/- 9.0 to 36.9 +/- 7.5 msec, and significantly altered the relationship between left ventricular pressure and dimension at end-diastole.

Animals↗

PubMed1984

Potential adverse effects of volume loading on perfusion of vital organs during closed-chest resuscitation.

To determine whether expansion of blood volume improves vital organ perfusion pressures and blood flow during closed-chest cardiopulmonary resuscitation in dogs, we recorded intracranial and high-fidelity ascending aortic and right atrial pressures and measured total and regional blood flow with radioactive microspheres during cardiopulmonary resuscitation before and after rapid infusion of 1 liter of saline or dextran in 12 animals. Volume loading increased total forward blood flow from 327.1 +/- 50.9 to 692.7 +/- 105.9 ml/min (p less than .01). However, blood flow to the cerebral hemispheres, cerebellum, brainstem, and ventricular myocardium all decreased significantly. For example, blood flow to the left cerebral hemisphere fell from 16.5 +/- 2.4 to 5.5 +/- 1.7 ml/min/100 g (p less than .001), while left ventricular myocardial blood flow fell from 12.0 +/- 3.1 to 4.1 +/- 0.8 ml/min/100 g (p less than .05). These changes in critical regional flow were accompanied by disproportionate increases in right atrial and intracranial pressures (relative to aortic pressure), which reduced the average pressure differences generated across the coronary and cerebral circulations from 11.0 +/- 2.5 to 3.7 +/- 1.3 mm Hg (p less than .01) and from 16.1 +/- 2.3 to 10.5 +/- 1.5 mm Hg (p less than .01), respectively. The overall rise in forward flow was associated with a marked increase in extracranial, brachiocephalic blood flow. These findings suggest that large increments in blood volume can reduce vital organ perfusion during cardiopulmonary resuscitation despite an increase in total forward blood flow.

Animals↗

PubMed1984

Volume-dependent effects of positive airway pressure on intracavitary left ventricular end-diastolic pressure.

To test the hypothesis that the effects of positive end-expiratory airway pressure (PEEP) on intracavitary left ventricular end-diastolic pressure (LVEDP) depend on the ventricular filling conditions under which PEEP is applied, the effects of PEEP on pressure in and around the left ventricle were determined before and after stepwise expansion of intravascular blood volume in 10 closed-chest dogs. Over a range of 0 to 20 cm of water, PEEP progressively increased both intrapericardial and intracavitary right ventricular end-diastolic pressures. These increases in pressure around the left ventricle were approximately linear and were relatively unaffected by volume loading. At the same time, PEEP always decreased transmural LVEDP by decreasing ventricular filling. However, transmural LVEDP fell more when ventricular volume was initially large, due to the nonlinear relationship between left ventricular transmural pressure and volume. As a result, intracavitary LVEDP (which reflected the sum of decreased transmural LVEDP and increased external pressure) increased when baseline ventricular volume was small and decreased when baseline ventricular volume was large. At intermediate volumes the fall in transmural pressure equaled the rise in external pressure, and intracavitary LVEDP did not change. These findings demonstrate that changes due to PEEP in intracavitary LVEDP are a complex function of increased intrathoracic pressure, decreased ventricular filling, and the operative level of left ventricular compliance.

Animals↗

PubMed1983

Effects of direct-current electrical shocks on systolic and diastolic left ventricular function in dogs.

Although direct-current (DC) electrical shocks do not significantly alter left ventricular systolic performance, their effects on ventricular diastolic properties and the role of sympathetic stimulation in maintaining postshock contractility are unknown. Accordingly, we studied both diastolic and systolic left ventricular performance in seven open-chest dogs before and after three consecutive 50 joule DC shocks applied directly to the heart. High-fidelity left ventricular pressure and segmental dimensions were recorded as pressure was varied systematically under conditions of beta-adrenergic blockade. The exponential left ventricular end-diastolic pressure-segment length relationship was not significantly altered by electrical shocks. Likewise, pre- and postshock beats matched for loading conditions did not differ in peak positive dP/dt, end-systolic segment length, or percentage of segment shortening, although mean normalized shortening rate decreased by approximately 11% (p less than 0.05). However, the time constant (T) for isovolumic pressure fall, an index of the rate of left ventricular relaxation, increased after shocks in all animals (T = 42.2 +/- 5.3 and 51.1 +/- 7.0 msec before and after shock, respectively; (p less than 0.01). We conclude that high-energy electrical shocks applied directly to the heart cause modest slowing of left ventricular relaxation but do not have important effects on left ventricular compliance or on systolic myocardial performance. These data suggest that DC shocks have only minor functional consequences when applied to normal hearts, even when sympathetic compensation is prevented.

Animals↗

PubMed1983

Effects of airway pressure and lung volume on left ventricular transmural pressure-volume relationships in humans.

Positive airway pressure, combined with increased lung volume, decreases left ventricular compliance in dogs. To determine whether airway pressure or lung volume influences left ventricular diastolic properties in humans, we examined two consecutive cineangiograms with simultaneous esophageal and left ventricular pressure recordings in 14 patients. Both studies were performed during sustained inspiration, one with atmospheric airway pressure, and one with positive airway pressure (9.1 +/- 2.4 mm Hg). Positive pressure caused higher transpulmonary (airway minus esophageal) pressure and therefore greater lung volume in 10 of 14 patients, while four patients had lower transpulmonary pressures due to decreased inspiratory effort. When positive airway pressure and increased lung volume were present together (n = 10), left ventricular transmural (ventricular minus esophageal) pressure-volume curves revealed higher transmural pressures at comparable diastolic ventricular volumes. For example, at end-diastole mean left ventricular transmural pressure was 25.2 +/- 12.9 mm Hg (compared to 20.8 +/- 12.3 mm Hg during control studies, p less than 0.05), while ventricular volume was unchanged (189 +/- 87 compared to 185 +/- 81 ml, p = NS). When all 14 patients were considered together, this effect was linked more closely to higher transpulmonary pressure than to positive airway pressure. We conclude that human left ventricular transmural pressure-volume relationships are influenced by airway pressure and lung volume. Our findings further suggest that lung volume may be more important than airway pressure in this regard.

Coronary Disease↗

PubMed1983

Thermodilution method overestimates low cardiac output in humans.

We compared 57 cardiac output measurements by the thermodilution and Fick methods in 26 patients and found that thermodilution values were higher in all 16 cases in which Fick outputs were less than 3.5 l/min. In 10 cases where Fick values were less than or equal to 2.5 l/min, thermodilution and Fick measurements differed by an average of 35%. When combined with the results of previous studies comparing the thermodilution, dye dilution, and Fick techniques, these findings suggest that the thermodilution method overestimates true cardiac output in the low output range. This overestimation probably is due to heat loss under conditions of low flow. Because the thermodilution method is used widely in patients with low output states, these findings have potentially important clinical implications.

Adolescent↗

PubMed1982

Relative lack of coronary blood flow during closed-chest resuscitation in dogs.

Recent studies have shown that blood flow during closed-chest cardiopulmonary resuscitation (CPR) results primarily from generalized changes in intrathoracic pressure rather than direct compression of the heart. Since ascending aortic and right atrial pressures rise and fall synchronously and to comparable levels during CPR, we hypothesized that the absence of a pressure difference across the coronary vascular bed during CPR precludes coronary blood flow. To test this hypothesis, we compared high-fidelity ascending aortic and right atrial pressures and carotid and coronary blood flow (electromagnetic flowmeters) during closed-chest CPR in 12 fibrillating dogs. Chest compression force was increased from 40 to 140 pounds in 20-pound increments using a pneumatic chest compression device. Although ascending aortic and right atrial pressures were always similar, high-compression-force CPR produced small mean pressure differences across the coronary vascular bed (5.6 +/- 0.8 mm Hg [+/- SEM] at 140 pounds). These pressure differences were accompanied by low levels of coronary blood flow. However, coronary flow was less than 1% control (prearrest) values whenever chest compression force was less than 100 pounds, and carotid flow exceeded coronary flow under all conditions (carotid and coronary flows at 140 pounds = 26.2 +/- 6.4% and 4.3 +/- 2.0% of prearrest values, respectively, p less than 0.01). We conclude that generalized changes in intrathoracic vascular pressures during closed-chest CPR promote carotid but not coronary blood flow. High-compression-force CPR produces small pressure differences across the coronary vascular bed, allowing low levels of coronary flow. However, even high-compression-force CPR is over six times more effective in maintaining carotid flow than coronary flow.

Animals↗

PubMed1981

Effects of exercise training on left ventricular mass in patients with ischemic heart disease.

To determine whether exercise training results in increased left ventricular mass in patients with ischemic heart disease, we obtained echocardiograms in 14 coronary patients before and after an average of seven months (range 3 to 14 months) of supervised arm and leg exercise. Each echocardiogram was interpreted jointly by two blinded observers, using three different measurement conventions and a semiautomated method of analysis to minimize errors of interpretation. Exercise training led to subjective improvement in all 14 patients, and to an objective increase in functional capacity in 13 of 14 patients, as evidenced by an increase in maximal oxygen consumption estimated from symptom-limited treadmill exercise testing (8.8 +/- 2.7 (SD) and 10.7 +/- 2.5 METS before and after training, respectively, p less than 0.01). However, this functional improvement was not accompanied by any significant change in left ventricular end-diastolic diameter, or posterior wall or interventricular septal thickness. Likewise, left ventricular cross-sectional area (CSA), an index of left ventricular mass which corrects for altered ventricular volume and theoretically reflects directional changes in mass despite nonuniform wall thickness, did not change significantly after training by any measurement convention (CSA = 18.0 +/- 6.5 and 17.6 +/- 6.5 cm2 before and after training, respectively, by American Society of Echocardiography measurements). These data strongly suggest that improved functional capacity after exercise training in patients with ischemic heart disease is not due to exercise-induced left ventricular hypertrophy.

Adult↗

PubMed1981

Reliability of echocardiographic and electrocardiographic parameters in assessing serial changes in left ventricular mass.

A reliable noninvasive index of left ventricular mass would be useful in following patients with valvular heart disease and left ventricular hypertrophy. We reviewed concurrent electrocardiograms and echocardiograms from 54 subjects, 39 patients with aortic or mitral valve disease and 15 normal subjects. Pre- and early postoperative echocardiographic estimates of left ventricular mass in 17 patients who had valve replacements correlated well (r = 0.96, p less than 0.001) and demonstrated little change in mean values despite altered left ventricular dimensions. Echocardiographic estimates of left ventricular mass were, therefore, used as a standard for evaluating other noninvasive indices. Precordial electrocardiographic voltage showed a weak correlation with left ventricular mass in the study group as a whole (r = 0.59, p less than 0.001), but no correlation in patients with volume overload (r = 0.36, p = NS). In 18 patients who had preoperative and three separate postoperative studies at least eight weeks apart, changes in left ventricular cross-sectional area (an index of left ventricular mass which corrects for changes in left ventricular volume) closely followed alterations in left ventricular mass. However, changes in posterior wall and interventricular septal thickness often resulted from altered ventricular volume and did not accurately reflect directional changes in left ventricular mass. Serial changes in electrocardiographic voltage were similarly unreliable. We conclude that left ventricular mass and cross-sectional area by echocardiography allow accurate noninvasive assessment of left ventricular mass, whereas wall thickness and electrocardiographic changes do not.

Cardiomegaly↗