Hemodynamic effects of pacing-induced tachycardia in valvular aortic stenosis.

The hemodynamic effects of tachycardia were studied in 13 patients with valvular aortic stenosis. Observations were made during sinus rhythm (average heart rate 80 beats/min) and two periods (P1 and P2) when atrial pacing increased the heart rate to 109 and 131 beats/min respectively. The cardiac index did not change, but the left ventricular stroke work index fell from 61.8 to 39.5 g X m/m2 (p less than 0.001) as the heart rate increased. The left ventricular end-diastolic pressure averaged 18 mm Hg during sinus rhythm and fell to about 11.5 mm Hg at P1 and P2 (p less than 0.001). The brachial arterial systolic pressure did not change during pacing, but the left ventricular systolic pressure fell from 208 mm Hg to 201 mm Hg during P1 (p less than 0.05) and 193 mm Hg during P2 (p less than 0.001). The mean systolic aortic valve gradient averaged 64 mm Hg during sinus rhythm and fell to 51 mm Hg during P2 (p less than 0.001), and the peak aortic valve gradient fell from 82 to 69 mm Hg during P2 (p less than 0.001). The left ventricular ejection time fraction increased from 26.9% during sinus rhythm to 31.9% during P1 (p less than 0.05) and 34.7% during P2 (p less than 0.005). Because of the prolonged left ventricular ejection time fraction and smaller stroke volume, a smaller pressure gradient developed across the stenosed valve at higher heart rates. The pacing test was of little value in assessing left ventricular function and thus is not useful during invasive investigations of valvular aortic stenosis.     

Recovery from heart failure: structural and functional analysis in a canine model

Chronic, rapid ventricular pacing produces congestive heart failure in the dog. Using echocardiography, the features of developing heart failure were analysed and the capacity of this model for recovery was assessed once pacing had been discontinued. Fifteen dogs were studied; nine were paced at 250 beats/min (bpm) to severe heart failure (5.0 +/- 1.8 weeks) and six served as sham controls. In the paced animals at severe heart failure, two-dimensional echocardiography demonstrated a significant increase in diastolic cross-sectional cardiac area (from 11 +/- 3 to 16 +/- 2 cm2, p less than 0.05), associated with a marked fall n area ejection fraction (54 +/- 8 to 21 +/- 8%, p less than 0.05), and significant left ventricular wall thinning (from 6.0 +/- 0.7 to 4.7 +/- 0.9 mm, p less than 0.05). In addition, significant increases in heart rate (77 +/- 7 to 126 +/- 13 bpm, sinus rhythm; p less than 0.05), respiratory rate (41 +/- 13 to 80 +/- 20 cycles/min, p less than 0.05), and body weight (21 +/- 1 to 24 +/- 3 kg, p less than 0.05) were noted. Serum sodium fell (146 +/- 3 to 140 +/- 8 mmol/L, p less than 0.05), while blood urea nitrogen (6 +/- 2 to 10 +/- 2 mmol/L, p less than 0.05) and creatinine (86 +/- 12 to 101 +/- 15 mmol/d, p less than 0.05) increased. Recovery was characterized by rapid improvement such that all measured parameters normalized by 1 week, except for cross-sectional cardiac area which remained dilated up to 4 weeks (14 +/- 3 cm2, p less than 0.05 versus control).(ABSTRACT TRUNCATED AT 250 WORDS)     

Human cardiovascular reactions to simulated hypovolaemia, modified by the opiate antagonist naloxone

Six healthy males were exposed to 20 mm Hg lower body negative pressure (LBNP) for 8 min followed by 40 mm Hg LBNP for 8 min. Naloxone (0.1 mg.kg-1) was injected intravenously during a 1 h resting period after which the LBNP protocol was repeated. Systolic, mean, and diastolic arterial blood pressures (SAP, MAP, DAP), and central venous pressure (CVP) were obtained using indwelling catheters. Cardiac output (CO), forearm blood flow (FBF), heart rate (HR), left ventricular ejection time (LVET), and electromechanical systole (EMS) were measured non-invasively. Pulse pressure (PP), stroke volume (SV), total peripheral resistance (TPR), forearm vascular resistance (FVR), systolic ejection rate (SER), pre-ejection period (PEP), PEP/LVET and indices for the systolic time intervals (LVETI, EMSI, PEPI) were calculated. During the second LBNP exposure, only two parameters differed from the pre-injection values: DAP at LBNP = 40 mm Hg increased from 60.0 +/- 4.8 mm Hg to 64.8 +/- 4.1 mm Hg (N = 4, p less than 0.02) and LVETI at LBNP = 20 mm Hg increased from 384.4 +/- 5.2 ms to 396.8 +/- 6.2 ms (N = 6, p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)     

Prolonged exercise induces left ventricular dysfunction in healthy subjects

To determine the effects of a moderately prolonged exercise on left ventricular systolic performance, 23 healthy male subjects, aged 18 to 51 yr (mean 37 yr) were studied. The subjects exercised first on a treadmill (brief exercise) and completed, on a separate day, a 20-km run. M-mode, two-dimensional, and Doppler echocardiography, as well as calibrated carotid pulse tracings, were obtained at rest and immediately on completion of both brief and prolonged exercise. Left ventricular systolic function was assessed by end-systolic stress-shortening relationships. Heart rate increased similarly after brief and prolonged exercise (+30%). Mean arterial pressure decreased from 99 +/- 7 to 92 +/- 8 mmHg (P less than 0.001) after prolonged exercise, but it remained unchanged after brief exercise. Left ventricular end-diastolic volume was decreased after prolonged exercise (130 +/- 23 vs. 147 +/- 18 ml at rest, P less than 0.01). Both ejection fraction and rate-adjusted mean velocity of fiber shortening decreased after prolonged exercise [from 67 +/- 5 to 60 +/- 6% (P less than 0.001) and from 1.12 +/- 0.2 to 0.91 +/- 0.2 cm/s (P less than 0.001), respectively] despite a lower circumferential end-systolic wall stress (133 +/- 23 vs. 152 +/- 20 g/cm2). The relationship between ejection fraction (or mean velocity of fiber shortening adjusted for heart rate) and end-systolic wall stress was displaced downward on race finish (P less than 0.05). These changes were independent of the changes in left ventricular end-diastolic volume and hence those in preload. The data suggest that moderately prolonged exercise may result in depressed left ventricular performance in healthy normal subjects.     

Role of exercise testing early after myocardial infarction in identifying candidates for coronary surgery.

It has been suggested that ST depression in lead V5 or equivalent on early exercise testing after acute myocardial infarction predicts a high risk of death. To evaluate exercise testing and radionuclide ventriculography in this context 103 consecutive patients with myocardial infarction who were able to undertake a limited exercise test before discharge from hospital were exercised and underwent gated blood pool scanning. No serious complications resulted from exercise testing. Twenty nine patients developed ST depression in lead V5, 19 had exertional hypotension, 31 developed a heart rate of greater than or equal to 130 beats/min, and 15 had complex ventricular arrhythmias. Death during the first year after discharge from hospital was associated with exertional hypotension (p less than 0.001) and a heart rate on exercise testing of greater than or equal to 130 beats/min (p less than 0.05); these two variables identified all nine deaths. Inability to complete the exercise protocol for any reason was also predictive of death (p less than 0.01). Ventricular arrhythmias and ST depression in lead V5 induced by exercise were not significantly associated with an increased risk of death. The mean (SD) radionuclide ejection fraction in the patients who died was 29 (16%) compared with 43 (11)% in the patients who survived (p less than 0.001). ST changes on exercise testing after myocardial infarction appear to be less predictive of later complications than haemodynamic signs, which may indicate left ventricular damage rather than ischaemia.     

Interrelationships between left ventricular volume and output during exercise in healthy subjects.

To better characterize the relationship between left ventricular volume response and improved ventricular ejection and output during supine exercise in normal subjects, 36 healthy asymptomatic volunteers (age 39 +/- 17 yr) were studied with radionuclide ventriculography during recumbent bicycle ergometry. Relative changes in left ventricular end-diastolic and end-systolic volume were measured at rest and during exercise by a modification of the radionuclide counts-based method that accounted for variability in stress blood pool counts. A biphasic response was noted in left ventricular end-diastolic volume with an initial increase in early exercise (8.5 +/- 11% at 200 kpm/min and 11 +/- 12% at 300 kpm/min) followed by a progressive and significant decline at peak exercise (-3.3 +/- 18% at 547 +/- 140 kpm/min; P < 0.05). There was substantial variation in end-diastolic volume response at peak exercise in the group as a whole, which could be more closely related to changes in end-systolic volume (r = 0.84, P < 0.0001) than in heart rate (r = -0.57, P < 0.01) or age (r = 0.36, P < 0.05) of the study subjects. Despite the decline in ventricular filling, systolic function appeared to improve dramatically at peak exercise (change in left ventricular ejection fraction 15.5 +/- 6.4, P < 0.0001). Although not directly related to increasing systolic ejection, end-diastolic volume was directly related to the percent change in stroke volume at peak exercise among the study subjects (r = 0.88, P < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Left ventricular function during graded exercise in patients with coronary artery disease and in control subjects.

The left ventricular function of 30 patients with coronary artery disease and 11 control subjects was studied by electrocardiography gated cardiac blood pool scintigraphy as the participants lay on their backs and either rested or exercised on a cycle ergometer at graded levels on intensity. The control subject showed a progressive increase in ejection fraction from rest (51% +/- 7%) to intermediate (56% +/- 10%, P less than 0.05) and maximum levels of exercise (64% +/- 10%, P less than 0.001). All the patients showed a decrease in ejection fraction from rest (42% +/- 16%) to their maximal level of exercise (36% +/- 11%, P less than 0.001). However, the response of some of the patients to intermediate exercise ranged from a decrease or no change to an increase in ejection fraction. Thus, exercise at maximal intensity is necessary to induce the left ventricular dysfunction that is diagnostic of coronary artery disease.     

Adaptation of the circulatory system to frequently repeated submaximal workloads in the light of left ventricular contraction analysis

In two groups of healthy men aged 20-22 years the left ventricular systolic time intervals were evaluated by the method of Weissler et al. during frequently repeated workloads and restitution. Each exercise was carried out on a Zimmerman cycle ergometer during 10 minutes, and was repeated five times at 50-minutes intervals from 8.00 o'clock a.m. Group I (15 subjects) performed the exercise at a stable workload which produced during the first exercise heart rate acceleration to 170/min, but gave a successive further rise in the heart rate during consecutive exercises. Group II (11 subjects) performed all exercises to a stable rise in heart rate to 170/min with decreasing workloads. It was found that successive exercises caused in both groups a similar decrease of the left ventricular ejection time index (LVETI), pre-ejection period (PEP), isovolumetric contraction time (ICT), and decrease of the PEP/LVET index (p less than 0.05). Each successive exercise began with higher values of LVETI, PEP, ICT and PEP/LVET than the first one. No significant differences were found in the values of left ventricular systolic time intervals in both groups (p greater than 0.05). The duration of restitution of normal values of the left ventricular systolic time intervals after successive exercises was not changing but the tolerance of these exercises measured by heart rate increase and work performed decreased successively.     

Ventricular pump function under ectopic excitation of the frog heart

The ventricular pump function under ectopic excitation of the heart was studied in decapitated and pithed adult frogs Rana temporaria (n = 21) at 18-19 degrees C. The intraventricular pressure was recorded with a catheter via ventricular wall. During pacing of the ventricular base and apex, the systolic pressure decreased (6.1 +/- 4.5 mm Hg and 8.9 +/- 5.0 mm Hg, respectively) as compared to the supraventricular rhythm (8.9 +/- 5.0 mm Hg, p < 0.05). The end-diastolic pressure decreased insignificantly both under basal and apical pacing. The systolic rate of pressure rise during dP/dtmax decreased under ventricular pacing, especially during pacing of the ventricular apex, as compared to the supraventricular rhythm (14.4 +/- 6/9 mm Hg/s and 22.1 +/- 11.2 mm Hg/s, respectively, p < 0.003). The isovolumetric relaxation (dP/dtmin) slowed during apical pacing as compared to the supraventricular rhythm (-25.1 +/- 13.6 and -35.6 +/- 18.3 mm Hg/s, respectively, p < 0.03). Ectopic excitation of the ventricular base and apex resulted in increase of the QRS duration (93 +/- 33 ms and 81 +/- 30 ms, respectively) as compared to the supraventricular rhythm (63 +/- 13 ms, p < 0.05). Thus, pacing of different ventricular areas ventricular myocardium with the ventricular pump function being reduced more obviously during the apical pacing compared to the pacing of ventricular base.     

Synergistic effects of a combined salbutamol-nitroprusside regimen in acute myocardial infarction and severe left ventricular failure.

The haemodynamic effects of a simultaneous infusion of salbutamol and nitroprusside were measured in 20 patients with acute myocardial infarction and severe left ventricular failure. Six patients also had clinical manifestations of cardiogenic shock. Ten patients received salbutamol first with the subsequent addition of nitroprusside; in the other 10 patients nitroprusside was infused first. Salbutamol was infused at a constant rate of 20 micrograms/min in all patients, while the dose of nitroprusside, which averaged 51.25 micrograms/min, was adjusted to reduce left ventricular filling pressure (measured as pulmonary artery end-diastolic pressure) to approximately 15 mm Hg with reference to sternal angle. Cardiac index increased in all patients from a mean of 1.8 to 2.6 l/min/m2 while pulmonary artery end-diastolic pressure fell significantly from 24 to 16 mm Hg. The adverse effects were small in most patients: heart rate did not increase significantly and systolic arterial pressure fell on average from 112 to 96 mm Hg. Ten of the 20 patients survived to leave hospital. Nitroprusside accounted for most of the fall in filling pressure irrespective of treatment sequence, whereas both drugs contributed to the augmented cardiac output. The haemodynamic benefits of this combined regimen were considerably greater than those achieved by either drug alone. Thus salbutamol and nitroprusside have synergistic effects which influence favourably the two principal manifestations of left ventricular dysfunction after extensive myocardial infarction.     

Volumetric responses of right and left ventricles during upright exercise in normal subjects

We evaluated the volumetric responses of the right and left ventricles to upright exercise using two noninvasive methods, first-pass radionuclide angiocardiography and the CO2 rebreathing technique, in nine normal subjects. Right (RV) and left (LV) ventricular ejection fractions, heart rate, and cardiac index were determined at rest and during steady-state exercise on the bicycle ergometer at 50% of maximal O2 consumption. From these data, stroke volume index (SVI), end-diastolic volume index (EDVI), and end-systolic volume index (ESVI) were derived. SVI increased from 40 +/- 7 ml/m2 at rest to 59 +/- 13 ml/m2 with exercise (P less than 0.001). RVEDVI increased significantly from 82 +/- 16 ml/m2 at rest to 95 +/- 21 ml/m2 during exercise (P = 0.008), while there was no significant change in RVESVI with exercise. Changes in LVEDVI and LVESVI during upright exercise were similar to the right ventricle. The increase in systolic blood pressure during exercise, along with no change in LVESVI, indicated enhanced ventricular contractility. The normal augmentation in SVI during submaximal exercise was due to both the Frank-Starling mechanism and an increased contractile state. Application of these or similar techniques may be useful in evaluating ventricular performance in patients with cardiorespiratory dysfunction.     

Cardiovascular effects of training for a marathon run in unfit middle aged men.

The effects of a 30 week exercise programme on serum lipid values, blood pressure, and cardiac function were assessed in a group of sedentary men aged 35-50 training for their first marathon. Mean serum cholesterol concentration (n = 33) fell by 12% from 6.54 (SE 0.18) to 5.76 (0.15) mmol/l (mean fall 0.78 mmol/l; 95% confidence interval 0.52 to 1.04 mmol/l), serum triglyceride concentration (n = 33) by 22% from 1.56 (0.17) to 1.21 (0.09) mmol/l (mean fall 0.34 mmol/l; 95% confidence interval 0.12 to 0.56 mmol/l), and mean blood pressure (n = 27) by 10% from 102 (2) to 92 (2) mm Hg (mean fall 10 mm Hg; 95% confidence interval 7 to 13 mm Hg). These changes were not explained by changes in body composition. Peak exercise left ventricular end diastolic volume (n = 16) increased with training; as a result of this and an increased exercise left ventricular ejection fraction peak exercise cardiac output increased from 19.9 (1.2) to 23.1 (3.0) l/min (mean rise 3.2 l/min; 95% confidence interval 1.5 to 5.0 l/min). Maximum oxygen consumption increased from 33.9 (1.6) to 39.0 (1.3) ml/kg/min (mean rise 5.0 ml/kg/min; 95% confidence interval 1.8 to 8.2 ml/kg/min). This study showed favourable effects on coronary risk factors and cardiac function and supports the place of regular exercise in coronary prevention programmes.     

Effect of using nifedipine by patients with chronic congestive heart failure treated with digoxin and furosemide

Nifedipine was administrated to 25 patients with chronic congestive heart failure treated with digoxin and furosemide++, nifedipine (NF) in a daily dose of 30-80 mg for 14 days. Before and after the treatment with nifedipine chest X-ray, blood biochemical investigations, echocardiographic evaluation of the left ventricular function and submaximal exercise test were performed. Nifedipine induced significant decreases in the left ventricular systolic dimension, heart volume, blood serum potassium and uric acid concentrations and hematocrit . Resting and exertional heart rate, blood pressure, exercise power and duration, watt-pulse, myocardial oxygen demand index, ejection fraction, cardiac output, body weight, 24-hour urinary output, blood serum concentrations of urea, creatinine, sodium and chloride changed insignificantly following nifedipine administration. The obtained results suggest that long-term nifedipine treatment of patients who were already given digoxin and furosemide neither improve nor worsen their clinical status.     

Clinical studies on aclacinomycin A cardiotoxicity in adult patients with acute non lymphoblastic leukaemia

Nine patients with acute non lymphoblastic leukaemia (ANLL) were treated with Aclacinomycin in the doses of 20 mg/m2/day x 7 days in 30' lasting intravenous infusion and Cytosin arabinosid 100 mg/m2/day x 7 days in continuous infusion as well as control group consisted of 30 healthy people were examined by means of 24 hrs Holter ECG monitoring and ultrasonocardiography (UCG) to evaluate the influence of Aclacinomycin A (Aclaplastin - Behring) on cardiac rhythm and function. The UCG and Holter examinations were performed before Aclacinomycin and after 7-10 days from the beginning of the therapy. There were no statistical differences between the results of UCG examination in Aclacinomycin-treated group before the therapy and the control group. A slight nonsignificant decrease in left ventricular stroke volume and ejection fraction were observed after Aclacinomycin. Cardiac index decreased after the therapy (p less than 0.05) but was of normal value. The only true significant (p less than 0.001) decrease was observed in the contractility of cardiac fibres but the cardiac failure was not observed. No alterations in left ventricular posterior wall and intraventricular septum thickness were found. The effusion to pericardium was observed in 2 pts in the initial study and in 1 of them also after the therapy. The obtained results supported the clinical observations that Aclacinomycin A is promising agent for the treatment of ANLL because of its low cardiotoxicity.     

Left ventricular hemodynamics during exercise recovery

The directional response of human left ventricular stroke volume during exercise recovery is unclear. Stroke volume has been reported to increase and decrease over exercise values during early recovery. The confounding variable may be posture. With the use of pulsed Doppler ultrasound, we tested the hypothesis that there is a significant difference between seated and supine stroke index (SI) during passive recovery from seated ergometer exercise. Thirteen subjects aged 26 +/- 2 yr performed two seated cycle ergometer exercise tests to 70% of predicted maximum heart rate (HR). Recovery was supine on one test and seated on the other. Cardiac index (CI), HR, and SI were calculated during rest, exercise, and 10 min of recovery. At rest, SI and CI were significantly (P less than 0.01) less and HR significantly (P less than 0.01) greater when the subjects were seated than when they were supine. At the last exercise work load, no significant differences were found in any measured variable between tests. During recovery, supine SI was maximal 180 s postexercise (99 +/- 14 ml/m2) and exceeded (P less than 0.01) resting supine (81 +/- 14 ml/m2) and peak exercise (77 +/- 14 ml/m2) SI by 22 and 29%, respectively. Seated SI was constant at peak exercise levels for 2 min. Seated and supine recovery CI never exceeded exercise values. Systolic and diastolic blood pressure recovery curves were similar in the two postures. We conclude that posture significantly affects SI during recovery from submaximal seated exercise. These results have implications for choice of recovery posture after stress testing in cardiac patients where it is desirable to minimize ventricular loading.     

Maintenance digoxin after an episode of heart failure: placebo-controlled trial in outpatients.

The need for maintenance digoxin treatment was assessed in a double-blind, variable-dose, crossover comparison with placebo. Forty-six outpatients who had been prescribed the drug for heart failure were studied; 33 were in sinus rhythm and the remainder in atrial fibrillation. Mean serum digoxin concentrations in those with sinus rhythm averaged 1-33 nmol/l, but a lower concentration, averaging 0-97 nmol/l, was accepted in those with atrial fibrillation as six of them developed bradycardia. Sixteen of the 46 patients deteriorated on placebo, and eight completely recovered when digoxin was reintroduced; in the remainder additional diuretics were required temporarily. Spirometric values deteriorated on changing to placebo whether or not the patient showed clinical evidence of recurrence of heart failure. In a separate study of nine patients who showed no clinical evidence of deterioration on placebo, reintroduction of digoxin caused a shortening of left ventricular ejection time, which persisted for at least a month. This suggests that the inotropic response to digoxin is sustained during maintenance treatment.     

Plasma levels and cardiovascular gene expression of urotensin-II in human heart failure

The peptide urotensin-II (U-II) has been described as most potent vasoconstrictor identified so far, but plasma values in humans and its role in cardiovascular pathophysiology are unknown. We investigated circulating urotensin-II and its potential role in human congestive heart failure (CHF). We enrolled control individuals (n=13; cardiac index [CI], 3.5+/-0.1 l/min/m2; pulmonary wedge pressure [PCWP], 10+/-1 mm Hg), patients with moderate (n=10; CI, 2.9+/-0.3 l/min/m2; PCWP, 14+/-2 mm Hg) and severe CHF (n=11; CI, 1.8+/-0.2 l/min/m2; PCWP, 33+/-2 mm Hg). Plasma levels of urotensin-II differed neither between controls, patients with moderate and severe CHF nor between different sites of measurement (pulmonary artery, left ventricle, coronary sinus, antecubital vein) within the single groups. Hemodynamic improvement by vasodilator therapy in severe CHF (CI, +78+/-3%; PCWP, -55+/-3%) did not affect circulating U-II over 24 h. Preprourotensin-II mRNA expression in right atria, left ventricles, mammary arteries and saphenous veins did not differ between controls with normal heart function and patients with end-stage CHF. In conclusion, urotensin-II plasma levels and its myocardial and vascular gene expression are unchanged in human CHF. Circulating urotensin-II does not respond to acute hemodynamic improvement. These findings suggest that urotensin-II does not play a major role in human CHF.     

Left ventricular function during arm exercise: influence of leg cycling and lower body positive pressure.

The purpose of this study was to characterize left ventricular (LV) diastolic filling and systolic performance during graded arm exercise and to examine the effects of lower body positive pressure (LBPP) or concomitant leg exercise as means to enhance LV preload in aerobically trained individuals. Subjects were eight men with a mean age (+/-SE) of 26.8 +/- 1.2 yr. Peak exercise testing was first performed for both legs [maximal oxygen uptake (Vo(2)) = 4.21 +/- 0.19 l/min] and arms (2.56 +/- 0.16 l/min). On a separate occasion, LV filling and ejection parameters were acquired using non-imaging scintography using in vivo red blood cell labeling with technetium 99(m) first during leg exercise performed in succession for 2 min at increasing grades to peak effort. Graded arm exercise (at 30, 60, 80, and 100% peak Vo(2)) was performed during three randomly assigned conditions: control (no intervention), with concurrent leg cycling (at a constant 15% leg maximal Vo(2)) or with 60 mmHg of LBPP using an Anti G suit. Peak leg exercise LV ejection fraction was higher than arm exercise (60.9 +/- 1.7% vs. 55.9 +/- 2.7%; P < 0.05) as was peak LV end-diastolic volume was reported as % of resting value (110.3 +/- 4.4% vs. 97 +/- 3.7%; P < 0.05) and peak filling rate (end-diastolic volume/s; 6.4 +/- 0.28% vs. 5.2 +/- 0.25%). Concomitant use of either low-intensity leg exercise or LBPP during arm exercise failed to significantly increase LV filling or ejection parameters. These observations suggest that perturbations in preload fail to overcome the inherent hemodynamic conditions present during arm exercise that attenuate LV performance.     

Anacrotic "notch" on the upstroke of external carotid curve may indicate a critically high systolic pulmonary arterial pressure value.

Acute respiratory failure is followed by decreased left ventricular performance probably due to the right ventricle dilatation induced by pulmonary hypertension and intraventricular septal shift to the left. An anacrotic notch on the upstroke slope of the carotid curve was detected in 22 of 36 hemodynamic studies with simultaneous ECG, PCG and external pulse carotid curve recording in 7 burned patients with acute respiratory failure. Comparing the values (x +/- SEM) obtained in group with notch and in group without notch, PAPs, PAPm, PVRI were higher (56 +/- 2.30 mmHg; 32 +/- 0.99 mm Hg; 543 +/- 56.8 dyn x s/cm5/m2 versus 32 +/- 1.08 mm Hg; 20 +/- 0.9 mm Hg; 173 +/- 14.7 dyn x s/cm5/m2) and CI and LVSWI were lower (2.6 +/- 0.17 l/min/m2; 25.8 +/- 2.41 g x m/m2; versus 3.8 +/- 0.26 l/min/m2; 38.3 +/- 2.82 g x m/m2) in group with notch. As it is shown by 11 paired measurements where the notch disappeared immediately after starting vasodilator therapy PAPs, PAPm, PVRI decreased (from 54 +/- 3.1, 35 +/- 0.8 mm Hg, 498 +/- 64.1 dyn x s/cm5/m2 to 35 +/- 0.8, 21 +/- 1.1 mmHg, 189 +/- 18.4 dyn x s/cm5/m2 respectively) and heart performance improved. Since the left ventricle contractility (characterized by EF, PCWP, ICT) was normal in both groups, our findings suggest that critically high PAPs values (over 40 mmHg) cause a septal bulging at the beginning of the systole which in turn narrows the left ventricle outflow tract. Regarding to the clinical importance of the deteriorated biventricular function at the critically high PAPs evidenced by notch phenomenon on carotid curve but measurable only by indwelling pulmonary arterial catheterization always being a source of infection, the noninvasive parameters as independent variables were entered into canonical discriminant analysis. The ratio of the correctly classified cases was 89%.     

Effect of endurance training on coronary artery size and function in healthy men: an invasive followup study

In eight healthy male volunteers (cardiologists; age 36 +/- 5 yr), bicycle spiroergometry, Doppler echocardiography, and quantitative coronary angiography with intracoronary Doppler measurements before and after completion of a physical endurance exercise program of >5 mo duration were performed. Maximum oxygen uptake increased from 46 +/- 6 to 54 +/- 5 ml x kg(-1) x min(-1) (P = 0.04), maximum ergometric workload changed from 3.8 +/- 0.3 to 4.4 +/- 0.3 W/kg (P = 0.001), and left ventricular mass index increased from 82 +/- 18 to 108 +/- 29 g/m(2) (P = 0.001). The right, left main, and left anterior descending coronary artery cross-sectional area increased significantly in response to exercise. Before versus at the end of the exercise program, flow-induced left anterior descending coronary artery cross-sectional area was 10.1 +/- 3.5 and 11.0 +/- 3.9 mm(2), respectively (P = 0.03), nitroglycerin-induced left coronary calibers increased significantly, and coronary flow velocity reserve changed from 3.8 +/- 0.8 to 4.5 +/- 0.7 (P = 0.001). Left coronary artery correlated significantly with ventricular mass and maximum oxygen uptake, and coronary flow velocity reserve was significantly associated with maximum workload.