Normal pulmonary circulation pressure values in healthy subjects at rest and during exercise

The paper is based on the results of an earlier retrospective international WHO study of normal pressure values in the pulmonary circulation and the right heart in 468 healthy individuals. The results of this study suggest that the pulmonary hypertension should be defined by the mean pulmonary artery pressure at rest of > or = 20 mmHg and not > or = 25 mmHg. Pulmonary wedge pressure should be < 12 mmHg. These results have recently been confirmed by the so far largest retrospective international study of normal values published by Kovacs et al and involving 1187 healthy volunteers. However, this study does not include pulmonary wedge pressure values. Normal values ofthe mean pulmonary artery pressure during exercise are determined by age. In healthy individuals younger than 50 years of age, the mean pulmonary artery pressure during exercise increases in parallel with increasing cardiac output. However, the increase in the mean pulmonary artery pressure during exercise is steeper in healthy individuals aged 50 years and over. This results from a sharper increase in the pulmonary wedge pressure caused probably by diastolic dysfunction of the left ventricle in the older population.     

Effect of digoxin on the electrocardiogram at rest and during exercise in healthy subjects

The effect of digoxin on the electrocardiogram at rest and during and after exercise was studied in 11 healthy subjects. Exercise was performed on a heart rate-controlled bicycle ergometer with stepwise increased loads up to a heart rate of 170 beats/min. The subjects were studied after peroral intake of digoxin at 2 dose levels and after withdrawal of digoxin. Administration of digoxin induced significant ST-T depression at rest and during exercise even at the small dose (2.4 +/- 0.8 microgram/kg body weight, mean +/- standard deviation). The ST-T changes were numerically small and dose-dependent. The most pronounced ST and T depression occurred at a heart rate of 110 to 130 beats/min. At higher heart rates the ST depression was less pronounced but still statistically significant. During the first minutes after exercise no significant digitalis-induced ST-T depression was seen. This reaction is not of the type usually seen in myocardial ischemia. Fourteen days after withdrawal of the drug there were no significant digitalis-induced ST-T changes at rest or during or after exercise.     

Echocardiographic and hemodynamic characteristics of reconstructed bicuspid aortic valves at rest and exercise

Summary Repair of diseased bicuspid aortic valves has gained increasing interest as an alternative to conventional valve replacement. Hemodynamic data at exercise have not been reported before. The aim of this study was to investigate the clinical and echocardiographic status of patients after bicuspid aortic valve repair at rest and exercise.Between 03/94 and 09/02 a reconstruction of an incompetent bicuspid aortic valve was performed in 25 patients (mean age 35±12.1 years, group A, mean insufficiency 2.8 preoperatively). Patients were investigated clinically and echocardiographically after 2.1±2.4 (0.1–8.9) years at rest and exercise and compared to 20 controls (group B). Clinical followup was complete. There were no deaths, reoperations, thromboembolic or bleeding complications. At last examination 21 patients were in NYHA class I, n=4 in NYHA class II and mean aortic valve insufficiency (AI) was 1.0 with one patient having an AI>II°.Maximum and mean pressure gradient (dPmax/mean) across the aortic valve at rest were 14±5.5/7±2.6 mmHg for patients of group A and 7±2.5/3.6±1.1 mmHg in group B. Mean AVA at rest was 2.6±0.8 (group A) vs 2.9±0.6 cm² (group B, p=0.025), valvular resistance 13.4±4.8 (group A) vs 13.6±2.9 dyn• s •cm^–5 (group B, p>0.05). All individuals were stressed up to 100 W (dPmax/mean 21±6.8/11±3.6, group A vs 11±2.9/6±1.3 mmHg, group B). 56% of group A and 85% of group B could be stressed up to 175 W with dPmax/mean 24.5±8.3/12±4.2 and 16±3.6/8±1.4 mmHg, respectively (p<0. 01). Heart rate and blood pressure behavior were comparable. Left ventricular mass regression (preoperatively 369.3±76.4 vs 277.3±80.7 g at last examination, p<0.01) was significant in group A but did not reach normal values (group B, 227.8±71.1; p<0.01).Bicuspid aortic valve reconstruction reduces left ventricular volume load significantly. Although residual mild subclinical obstruction and incompetence were observed, the behavior of hemodynamics at exercise was comparable to controls. The clinical relevance of these findings in long term follow-up has to be evaluated.     

Echocardiographic and hemodynamic characteristics of reconstructed bicuspid aortic valves at rest and exercise

Repair of diseased bicuspid aortic valves has gained increasing interest as an alternative to conventional valve replacement. Hemodynamic data at exercise have not been reported before. The aim of this study was to investigate the clinical and echocardiographic status of patients after bicuspid aortic valve repair at rest and exercise.Between 03/94 and 09/02 a reconstruction of an incompetent bicuspid aortic valve was performed in 25 patients (mean age 35±12.1 years, group A, mean insufficiency 2.8 preoperatively). Patients were investigated clinically and echocardiographically after 2.1±2.4 (0.1–8.9) years at rest and exercise and compared to 20 controls (group B). Clinical followup was complete. There were no deaths, reoperations, thromboembolic or bleeding complications. At last examination 21 patients were in NYHA class I, n=4 in NYHA class II and mean aortic valve insufficiency (AI) was 1.0 with one patient having an AI>II°.     

Subacute hemodynamic effects of nebivolol in man at rest and during exercise

In a subacute experiment 7 apparently healthy volunteers received a daily oral dose of 5 mg nebivolol for seven days, followed by a seven-day washout period with placebo. From the first day during treatment with nebivolol, peak exercise heart rate and systolic blood pressure, as measured during a standardized submaximal treadmill exercise, significantly decreased by 15% and 19% respectively. A prolonged treatment for one week did not further increase the response of exercise heart rate and systolic blood pressure to nebivolol. However, the ratio of preejection period (PEPc) to left ventricular ejection time (LVETc), an indirect and valuable measure of left ventricular performance, progressively and significantly decreased during the seven-day treatment period with nebivolol from a mean value of 0.37 +/- 0.012 to 0.31 +/- 0.009. The improvement of systolic time intervals resulted from a shortening of the PEPc and a lengthening of the LVETc. At rest, heart rate did not change significantly with nebivolol, whereas both systolic and diastolic blood pressure gradually and significantly lowered. The postexercise LVETc significantly shortened during treatment with nebivolol, and this shortening was more pronounced after seven days of treatment. After discontinuation of treatment with nebivolol, all these effects persisted for more than thirty hours after the last intake and gradually returned to pretreatment values thereafter. From these data it appears that nebivolol effectively reduces blood pressure at rest and during exercise in healthy volunteers, beneficially influencing preload and afterload, as measured by systolic time intervals.(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute effects of alcohol on left ventricular function in healthy subjects at rest and during upright exercise

Six healthy men, aged 23 to 30 years, were studied by radionuclide angiocardiography at rest and at 2 submaximal exercise levels in the upright position during increasing alcohol intoxication. At light intoxication (serum ethanol 23 mmol/liter), the median value of left ventricular (LV) ejection fraction (EF) at rest decreased by 5%. At heavy intoxication (serum ethanol 45 mmol/liter), the median LVEF decreased at rest by 11% and during 75% submaximal exercise by 6%, heart rate at rest increased (median 81 vs 62 beats/min), and systolic blood pressure decreased during 50% submaximal exercise (median 145 vs 163 mm Hg). No significant changes of plasma epinephrine concentrations were recorded, whereas plasma norepinephrine concentrations were increased by 24% at rest during light intoxication and by 30 to 38% during heavy intoxication. No changes of LVEF and plasma catecholamine levels were recorded after ingestion of isovolumic, isocaloric drinks as compared with values obtained before intake. Thus, influences of ingestion per se and repeated investigations of LV function were excluded. These findings suggest that in healthy subjects alcohol intoxication causes a dose-dependent impairment of cardiac contractility. Compensatory mechanisms may account for a reduced influence during exercise.     

Hemodynamic effects of disopyramide at rest and during exercise in normal subjects

The hemodynamlc effects of disopyramide phosphate, 2.0 mg/kg body weight, given intravenously over a period of five minutes were studied at rest and during exercise in ten patients without clinical or anglographlc evidence of heart disease. Following disopyramide, the resting cardiac index was lower (4.0 ± 0.6 vs 4.3 ± 0.6 iners/min/m², mean ± 1 SO, P <0.05), while left ventricular end-dlastollc pressure (16 ± 4 vs 11 ± 4 mm Hg, P <0.001), pulmonary arterial (PA) mean pressure (20 ± 5 vs 17 ± 5 mm Hg, P <0.05), and brachlal arterial (BA) mean pressure (105 ± 8 vs 96 ± 7 mm Hg, P <0.05) were higher than the pre-infuslon resting values. During exercise, there was no change in left ventricular end-diastollc pressure while cardiac index rose from 4.0 ± 0.6 to 6.5 ± 0.6 itters/mln/m² (P <0.001) and left ventricular stroke work index increased from 62 ± 19 to 84 ± 22 gm/beat/m² (P <0.001). The normal hemodynamlc response during exercise after disopyramide despite the apparent depression of left ventricular function at rest probably reflects the positive inotroplc effect of enhanced sympathoad-renergic activity.     

Acute hemodynamic effects of nifedipine at rest and during stress in severe aortic incompetence

To determine whether afterload reduction with nifedipine iseffective both at rest and during stress tests (rapid atrialpacing and contrast material overload), 14 patients with chronicsevere isolated aortic insufficiency (10 asymptomatic) underwentright and left cardiac catheterization. Forty-five minutes after 20 mg of nifedipine (sublingually),left ventricular end-diastolic pressure, peak aortic pressure,systemic vascular resistance and double product decreased significantlyat rest, at peak paced rate, and after angiography (P valuesfrom <0.05 to <0.001). Cardiac index increased at restingheart rate (P<0.01) but was unchanged during pacing. Thereduction of systemic vascular resistances was inversely correlatedwith its initial value (r = –0.69). After nifedipine, average regurgitant fraction did not change;however its variations were significantly correlated with thoseof systemic vascular resistance (r = 0.69). It is concluded that in severe aortic insufficiency, nifedipineinduces an effective reduction of left ventricular pre- andafterload, accompanied by an enhanced mechanical efficiency(unchanged or increased cardiac index with lower double product),both at rest and during stress tests.     

Hemodynamic and hormonal abnormalities in canine aortic coarctation at rest and during exercise

This study was designed to determine the hemodynamic and hormonal consequences of aortic coarctation at rest and during treadmill exercise. Twelve normal adult dogs served as controls. In eight dogs coarctation was created within 1 week of birth by banding the aorta just proximal to the ductus ligament, thereby fixing luminal diameter at 1 to 2 mm. Studies were performed 18 months after operation. Vascular pressures were monitored proximal and distal to the coarctation, cardiac output and regional blood flow were evaluated with radioactive microspheres and blood samples were collected for determination of hormone levels and blood gases. At rest, systolic pressure in the proximal aorta was 130 +/- 12 mm Hg (mean +/- SD) in the control group and 167 +/- 16 mm Hg in dogs with coarctation (p less than 0.01). During exercise at a level that doubled heart rate and cardiac index, mean aortic pressure increased by 11 and 31% (p less than 0.01) in the control and the coarctation group, respectively. Mean distal aortic pressure increased by 8% during exercise in control dogs but decreased by 29% in dogs with coarctation. Exercise decreased flow to the kidneys and the large intestine in the coarctation group. Plasma norepinephrine concentrations were greater in the coarctation group than in control dogs at rest; during exercise, plasma norepinephrine, epinephrine and renin activity increased in both groups, but to a greater degree in the group with coarctation. These results confirm an abnormality in renal and gut perfusion in experimental coarctation and suggest that this may be related to a decline in perfusion pressure.(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute and long-term hemodynamic effects of tiapamil at rest and during exercise in essential hypertension

Summary The first dose and long-term hemodynamic responses to tiapamil—an aralkylamide calcium- channel blocker—were studied both at rest and during exercise in 18 male patients (mean age, 45 years) with essential hypertension (EH). Blood pressure (BP) was measured intra-arterially, cardiac output (CO) was measured by dye dilution and heart rate (JR) was measured by electrocardiogram. One hour after the first oral dose of 600 mg tiapamil, mean arterial pressure (MAP) fell 14%. Total peripheral resistance (TPR) fell 21%, while HR and CO increased 7% and 11%, respectively. There-after the effects leveled off. After 11 months of chronic tiapamil therapy (mean dose 980 mg per day), MAP was reduced 11% at rest sitting. The reduction in BP was associated with a modest reduction in TPR. Similar responses were seen at rest supine and during 100-W bicycle exercise. A small reduction was seen in HR while CO was preserved. In conclusion, tiapamil exerts a moderate antihypertensive effect, both at rest and during exercise, through reduction of TPR without a fall in heart pump function. The long-term hemodynamic changes are rather similar to those of verapamil.     

Certain hemodynamic indicators during rest and after intensive physical exercise at high altitude]

For 5 years 364 normal males, aged 19--25, were studied at the altitude of 3800--4200 m, along with local inhabitants of the mountain region; the hemodynamic shifts and arterial blood oxygenation were studied with the base metabolism conditions preserved both at rest, and after intensive physical exercises performed according to the step-test method with the maximum tempo of the work (cardiological motion test, WHO, 1967). The initial reaction of the cardiovascular system to the high altitude conditions manifested itself in an increased stroke volume and cardiac output, of the volume speed of blood ejection, of the cardiac index in a decrease of the total peripheral resistance and oxygen saturation of the arterial blood. This reaction was interpreted as a compensatory one. In the course of acclimatizing, the cardiac output and the pulse amplitude of the arterial pressure gradually decreased, and the total peripheral resistance increased. These hemodynamic changes must be of an adaptative nature. The maximum physical workload caused a distinct intensification of the circulatory reactions, especially in those living for considerable periods of time at high altitude and in local inhabitants. The general state of the examined remained good. Hence, these persons have a considerable reserve of functional capacities of their cardiovascular system, and can perform hard muscle work at high altitude. Individuals staying at high altitude for only short periods of time react to intensive physical workloads by a less distinct intensification of the contractile capacity of the heart and by a sharp decrease of blood oxygenation, considerable acceleration of the heart rate and respiration rate, as well as by a deterioriation of their general state. Such muscular efforts cause overloading of the heart only in persons with a short-term acclimatizing.     

Right ventricular function at rest and during exercise in aortic and mitral valve disease

Right ventricular function at rest and during exercise was examined in a group of patients with symptomatic aortic or mitral valve disease, or both. The right ventricular ejection fraction was less than 45% in 22 of 36 patients at rest and in 12 of 17 subjects at symptom-limited, supine bicycle exercise. The right ventricular ejection fraction failed to increase more than 5% with exercise in 17 of 17 patients. The central venous pressure was greater than 5 mm Hg in 18 of 36 patients at rest and in 13 of 17 patients at maximal exercise. There was a significant inverse relation between rest right ventricular ejection fraction and mean pulmonary artery pressure (r = -0.47, p less than 0.05) and between rest right ventricular ejection fraction and mean central venous pressure (r = -0.39, p less than 0.05). There was no significant relation between the exercise values of these variables. In individual patients, the changes in right ventricular ejection fraction and pulmonary artery pressure with graded exercise were nonlinear. It is concluded that right ventricular function is not a simple function of pulmonary artery pressure at rest or during exercise in aortic and mitral valve disease. Less than one-quarter of the variation in right ventricular ejection fraction at rest can be explained by the variation in pulmonary artery pressure, and the finding of a normal (greater than 45%) right ventricular ejection fraction does not reliably exclude the possibility of pulmonary hypertension in a patient with valvular heart disease.     

Comparison of hemodynamics during hyperthermal immersion and exercise testing in apparently healthy females aged 50-60 years.

BACKGROUND: Owing to excessive worries regarding adverse cardiac events, hyperthermal balneotherapy for patients with coronary artery disease is underprescribed. However, very few cardiac events occur in similar heat stress during Finnish sauna bathing. Exercise testing has proven to be a safe diagnostic procedure even in survivors of myocardial infarction. METHODS: We compared the effects of hyperthermal immersion and exercise testing on cardiac hemodynamics in 21 apparently healthy women aged 50-60 years. The maximal symptom-limited bicycle exercise test was performed according to the modified protocol of Wasserman. Hyperthermal immersion was carried out in 40 degrees C water and was completed by increasing the core temperature by about 2 degrees C. The left ventricular function was evaluated using continuous measurement of thoracic electric bioimpedance during both tests. The blood pressure, index of contractility and heart rate were measured directly, whereas the cardiac index, left cardiac work index and systemic vascular resistance index were calculated. RESULTS: The hemodynamic response, as assessed at continuous non-invasive monitoring, showed substantial differences between hyperthermal immersion and exercise testing. Overall, we found a significantly lower hemodynamic load during hyperthermal immersion in comparison with exercise testing. Entering the bath, there was a significant decrease in the left cardiac work, contractility and blood pressure. We recorded a slight increase in the heart rate towards peak hyperthermal immersion. However, other modulators such as the mean arterial pressure, index of contractility, cardiac index and left cardiac work index decreased even below resting values. CONCLUSIONS: Excessive hyperthermal immersion induced a lower hemodynamic load in apparently healthy women than standard maximal exercise testing.     

The cardiovascular response at rest and during exercise in hypothyroid subjects to thyroxine substitution

Rapid and intense thyroxine substitution can lead to heart failure and myocardial infarction in hypothyroid patients. We have analyzed the normalization of the circulatory system in hypothyroid subjects on a gradual thyroxine substitution. Fourteen hypothyroid patients were studied repeatedly with an orthostatic test and a standardized symptom-limited exercise test during substitution. ST and T abnormalities were observed in 51 and 33%, respectively, before substitution. Many of these changes were normalized upon substitution at a dose level of 0.15 mg/d thyroxine. The pulse reaction to standing was enhanced early during substitution. The capacity to perform work, on the other hand, responded more slowly to thyroxine substitution, and was significantly increased only after six months of full substitution. This difference in the time course of recovery may be of clinical importance when substituting patients with hypothyroidism and ischemic heart disease.     

Effects of nifedipine and diltiazem on hemodynamic responses at rest and during exercise in hypertensive patients

Twelve patients with uncomplicated systemic hypertension were treated with nifedipine (30 mg/day) and diltiazem (180 mg/day) for 1 month each, and performed two stage (50 watt and 100 watt) of bicycle ergometer exercise before and after each period of administration. Both drugs produced significant reduction in systolic and diastolic blood pressure at rest and during exercise, while the mean values of systolic blood pressure tended to be less with nifedipine than with diltiazem. Nifedipine caused a nonsignificant increase in heart rate at rest and during exercise, but diltiazem significantly decreased it at rest and during exercise. Cardiac output was significantly increased at rest and during mild exercise (50 watt), but not during more strenuous exercise (100 watt) with both drugs. Thus, different actions in arterial vasodilation and chronotropism between nifedipine and diltiazem in usual clinical doses were noted. However, nifedipine and diltiazem may be effective in hypertensive patients, probably with left ventricular dysfunction, because both drugs reduced systemic blood pressure even during exercise with simultaneous increase in cardiac output at rest and during mild exercise.