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Onset of intolerance symptoms during exercise testing is a reproducible threshold for evaluation of cardiac function.

Twenty-one male patients with a history of myocardial infarction underwent bicycle cardiopulmonary exercise testing. The onset of leg pain or dyspnea, which reflects anaerobic metabolism, was termed anaerobic exercise symptom threshold (AEST). Our aims were (1) to evaluate the temporal relationship between AEST and the ventilatory anaerobic threshold (VAT) and (2) to determine whether heart rate, rate-pressure product, exercise time, and the ventilatory parameters at AEST are reproducible and correlate with the same parameters at VAT. AEST overlapped VAT in 4 patients and lagged behind VAT in 15. AEST never preceded VAT. The mean exercise time at VAT was 4.1 +/- 1.2 min and at AEST 5.6 +/- 1.6 min (p < 0.0001); the mean heart rate was 97 +/- 10 and 107 +/- 12, respectively (p < 0.001). The mean values of the rate-pressure product and the oxygen consumption at AEST were significantly higher than at VAT. The correlation coefficient ranged from r = 0.74 to r = 0.93. Fifteen patients were examined twice within 1 month; the above parameters were reproducible at AEST, VAT, and peak exercise. In conclusion, AEST, which is easily recorded during bicycle exercise testing, is useful as a reference point for evaluation and follow-up of the cardiac aerobic function.

Anaerobic Threshold↗

Exercise training enhances cardiac function in response to an afterload stress in older men.

This study was designed to characterize cardiac adaptations to endurance exercise training in older healthy men by evaluation of changes in left ventricular function in response to an afterload stress in the presence of cardiac muscarinic receptor blockade. Eight men 65 +/- 2 (SE) yr old underwent 9 mo of endurance exercise training. Maximal O2 uptake (V(O2 max)) was determined during treadmill exercise. Left ventricular function was assessed with two-dimensional echocardiography and pulsed Doppler transmitral flow velocity profile at baseline, after an intravenous bolus of atropine and during infusion of graded doses of phenylephrine. V(O2 max) was increased by 29% in response to training (28.9 +/- 1 to 37.3 +/- 1 ml x kg(-1) x min(-1)). Baseline end-diastolic diameter (EDD) was increased, with no change in left ventricular wall thickness-to-radius ratio, after training, suggestive of eccentric left ventricular hypertrophy. EDD, end-systolic dimension, and end-systolic wall stress (sigma(es)) increased similarly in response to phenylephrine before and after training. Fractional shortening (FS) decreased in response to phenylephrine before but not after training. When the changes in FS (delta FS) during phenylephrine infusion were plotted as a function of changes in sigma(es), delta FS were significantly higher after than before training (P = 0.003) at comparable increases in sigma(es), indicative of improved contractile function. This adaptive response was preload independent, because EDD did not differ between the trained and untrained states during phenylephrine infusion. Heart rate responses to phenylephrine were similar before and after training. Exercise training resulted in a higher (P = 0.028) early-to-late transmitral diastolic flow velocity ratio at virtually identical heart rates, suggestive of improved diastolic filling. The results suggest that endurance exercise training induces an enhancement of left ventricular systolic function in response to an afterload stress in older healthy men.

Aged↗

Cardiac function in rats with acute renal failure.

Inotropic responses of isolated cardiac preparations from rats with glycerol-induced acute renal failure (ARF) were recorded, following a range of cardiac stimulants. Left atria of rats with ARF showed diminished inotropic responses only to the calcium agonist Bay K 8644 (methyl 1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoromethyl-phenyl)-pyridine-5 -carboxylate) whilst right ventricular strips exhibited reduced responses to isoprenaline, 3-isobutyl-1-methylxanthine, Ca2+ and Bay K 8644. Investigations of cardiac mitochondrial respiration indicated that there is a site-unspecific 'pseudo' uncoupling of oxidative phosphorylation in ARF but that electron transport is unaffected. This uncoupling of oxidative phosphorylation did not have any detectable effect on either levels of total adenine nucleotides and creatine phosphate or cellular energy charge. Measurements were also made of the activity of pyruvate dehydrogenase which provides an index of mitochondrial Ca2+ levels. The proportion of pyruvate dehydrogenase in its active form was threefold higher following isoprenaline injection in hearts of rats with ARF compared with controls. The results suggest that in hearts of rats with ARF there is a change in the number, affinity, efficacy or coupling of the dihydropyridine receptor on the L-type calcium channel. Moreover, in the ventricle, a defect in cellular Ca2+ control, resulting in an increase in mitochondrial Ca2+ uptake, may contribute to the depression of inotropic response to the range of cardiac stimulants tested.

1-Methyl-3-isobutylxanthine↗

Passive effect of reduced cardiac function on splanchnic intravascular volume.

It has been hypothesized that lowered cardiac output due to heart failure results in passive redistribution of intravascular volume from the peripheral circulation to the central circulation and that this redistribution acts to support cardiac output. To test this hypothesis, acute heart failure was induced by rapid atrial pacing to raise heart rate from 148 +/- 6 to 232 +/- 1 beats/min for 5 min, while splanchnic intravascular volume was assessed with radionuclide imaging in eight anesthetized pigs that had undergone prior carotid denervation and vagotomy. Cardiac output decreased from 3,350 +/- 410 to 2,170 +/- 290 ml/min (P less than 0.001), mean arterial pressure decreased from 103 +/- 5 to 84 +/- 4 mmHg (P less than 0.001), left atrial pressure increased from 5.9 +/- 0.6 to 10.8 +/- 0.9 mmHg (P less than 0.001), right atrial pressure increased from 2.4 +/- 0.5 to 4.8 +/- 0.9 mmHg (P less than 0.001), total splanchnic intravascular volume did not change (0 +/- 2 ml), splenic intravascular volume decreased 11 +/- 3% (P less than 0.001), hepatic intravascular volume increased 12 +/- 2% (P less than 0.001), and mesenteric intravascular volume did not change (-3 +/- 2%). Thus, when cardiac output is lowered with pacing-induced acute heart failure, lowered perfusion pressure acts to lower splenic intravascular volume and increased central venous pressure acts to increase hepatic intravascular volume; however, total splanchnic intravascular volume does not decrease to support cardiac filling and cardiac output.

Animals↗

Effects of hydralazine on streptozotocin-induced diabetic rats: prevention of hyperlipidemia and improvement in cardiac function.

The effects of hydralazine on blood lipids, systolic pressure and cardiac performance were assessed in male Wistar rats, 6 weeks after they were made diabetic with streptozotocin (STZ). STZ-induced diabetes results in a loss of body weight, hyperglycemia and hypoinsulinemia. These effects are not altered after hydralazine treatment. STZ-diabetes also produced a significant bradycardia, elevation of blood pressure, hyperlipidemia and decreases in the levels of triiodothyronine and thyroxine. Hydralazine treatment successfully prevented all these alterations. In addition, cardiac performance was depressed in the untreated diabetic animals, but the cardiac performance of the hydralazine-treated diabetic animals showed a definite improvement. Thus, hydralazine controlled the high serum lipids and blood pressure and improved cardiac performance in STZ diabetic rats.

Animals↗

[Cardiac functions].

Explore the source record for details and available documents.

Adenosine Triphosphate↗

Reliability of noninvlasive methods for measuring cardiac function in exercise.

Externally recorded systolic time intervals (STI's), indirect (CO2 re-breathing) cardiac output, and auscultatory blood pressures were measured during upright bicycle ergometer work in 20 healthy men, aged 24-56 yr. The subjects were studied on 2 separate days at steady-state work loads chosen to represent light (mean heart rate (HR) = 96 beats.min-1), moderate (HR = 118 beats.min-1) and heavy (HR = 147 beats.min-1) exercise. In addition to determinations of cardiac output, systolic time intervals, and blood pressure, the individual's mean systolic ejection rate (stroke volume/left ventricular ejection time) was calculated as a measure of left ventricular function. In general, heart-rate-corrected STI's were found to be reliable and reproducible. Reliability coefficients for total electromechanical systole and left ventricular ejection time ranged from 0.93 to 0.96 while those for the preejection period and its subcomponents were between 0.63 and 0.88. The reliability of cardiac output, stroke volume, mean systolic ejection rate, and systolic blood pressure was also considered to be acceptable but tended to be higher during moderate and heavy work (r = 0.85-0.95) compared to light exercise (r = 0.60-0.83).

Blood Pressure Determination↗

Cocaine: a review of its toxic actions on cardiac function.

It has become increasingly apparent that cocaine abuse can provoke lethal cardiac events, including myocardial infarction and ventricular fibrillation. The mechanisms responsible for these cardiotoxic actions of cocaine largely remain to be determined. Cocaine has two primary pharmacological properties that can adversely affect the heart and vasculature. Cocaine acts both as a local anesthetic (sodium and potassium channel blockade) and as a powerful cardiac stimulant that accentuates the actions of the sympathetic nervous system (inhibition of central and peripheral neuronal catecholamine uptake). The local anesthetic properties could impair impulse conduction, as well as elicit inhomogeneities in repolarization (refractory period), which creates an ideal substrate for reentrant arrhythmias. In addition, high doses of cocaine can depress contractile function due to inhibition of sodium/calcium exchange that results from decreased sodium influx (local anesthetic action). These actions are particularly obvious when sympathomimetic effects of cocaine are blunted. In a similar manner, the cocaine-induced accumulation of catecholamines potentiates the activation of alpha- and beta-adrenergic receptors, which can provoke coronary vasospasm (myocardial ischemia and infarction), increased contractile force (increased metabolic demand), and cardiac arrhythmias. The activation of adrenergic receptors will elicit a cascade of second messengers, ultimately provoking an increase in cytosolic calcium. These elevations in cytosolic calcium can provoke oscillations in membrane potential, triggering sustained action potential generation and extrasystoles. In particular, activation of the alpha IA-adrenergic receptor subtype and corresponding increase in calcium influx via voltage sensitive (L type) channels may play a critical role in the genesis of malignant arrhythmias. Thus, the adrenergic and local anesthetic properties of cocaine could act synergistically to elicit toxic actions on the heart.

Animals↗

Bromocriptine for an acromegalic patient. Improvement in cardiac function and carpal tunnel syndrome.

A 64-year-old woman with active acromegaly of 33 years' duration, severe carpal tunnel syndrome, and subclinical heart disease was treated with bromocriptine mesylate. Within eight months of therapy, basal growth hormone (GH) levels decreased from 90.0 to 7.0 ng/mL, and hand volume was reduced from 375 to 295 mL. Concomitantly, echocardiographic studies showed normal left ventricular size and function. Electromyographic studies demonstrated normal function in both median nerves. Bromocriptine may correct cardiac dysfunction and carpal tunnel syndrome in acromegaly either by reduction of GH oversecretion or by a direct effect of bromocriptine on dopamine receptors in the heart and peripheral nerve endings.

Acromegaly↗

Long-term evaluation of cardiac function in obese patients treated with a very-low-calorie diet: a controlled clinical study of patients without underlying cardiac disease.

Twenty obese women were randomly assigned to consume (for 16 wk) either a 420-kcal/d liquid diet (n = 12) or a 1200-kcal/d balanced diet (n = 8). Thereafter, patients in both conditions were prescribed a 1200-kcal/d diet for the remainder of treatment (week 45). Six obese nondieters served as control subjects. Ambulatory electrocardiographic (Holter) monitor readings were obtained on all patients at baseline and weeks 3, 9, 13, 17, 19, and 45 of the study and were analyzed for ventricular premature depolarizations (VPDs) per hour, paired forms, and runs of ventricular tachycardia. There were no statistically significant changes in VPDs in any condition during treatment. Similarly, there were no significant changes in the PR, QRS, and corrected QT intervals. The results indicate that under appropriate medical supervision, very-low-calorie diets can be used safely for up to 16 wk by significantly obese patients free of pre-existing cardiac disease.

Diet, Reducing↗

Cardiac function, morphology and chromosomal aberrations in a calf with ectopia cordis cervicalis.

A male calf with ectopia cordis cervicalis inferior was investigated clinically, hemodynamically, and morphologically from the 3rd day of age until slaughter at the age of 22 months. Arterial hypertension (mean AOP 140 mm Hg), concentric myocardial hypertrophy and good ventricular contractility with normal valve function were found. Normal clinical condition at rest (cardiac output 48 l/min in the 600 kg bullock), but cyanosis and dyspnea during physical exercise were observed. Variations in the large vessels, such as persistence of the right cranial caval vein and one common pulmonary vein emptying into the left atrium, were found. Abrupt caliber differences of large arterial vessels together with a right angled aortic arch were observed, presumably contributing to increased afterload. The cytogenetic analysis showed the presence of a small marker chromosome leading to a chromosome number of 61 in a fraction of metaphases (mosaicism). Moreover, chromosome breakages were observed in many cells. From the 5 cows which were inseminated, 3 became pregnant. Ectopia cordis was not observed in any offspring. We conclude that in this animal compensated cardiac insufficiency with peripheral hypertension was established.

Animals↗

[The effect of hypothyroidism on cardiac function in dogs].

The thyroid hormones have direct and indirect effects on the heart. So it is possible that depression of left ventricular function is associated with hypothyroidism. This publication describes cardiac findings (auscultation, electrocardiography, echocardiography) in ten hypothyroid dogs. Low heart rates, reduced R-amplitudes and bradycardic arrhythmias (first and second-degree AV block) were found on the electrocardiogram before treatment. On the echocardiograms most of the dogs showed reduced contractillity and reduced left ventricular wall thickness. Seven dogs were reexamined after levothyroxine supplementation. Effects of treatment were increased heart rates and R-amplitudes as well as disappearance of the bradycardic arrhythmias in electrocardiographic examination. The echocardiographic examination showed increased contractility and increased left ventricular wall thickness.

Animals↗

Cardiac function, fiber shortening, and dynamic geometry.

Many models for the study of the pump function of the heart emphasize the importance of cardiac geometry and detailed dimensional data. Because of the lack of accurate measuring techniques, approximate geometries such as shells of revolution have been applied. In this study, methods are presented that measure the dynamic geometry of the working, isolated canine heart by means of ultrasound-velocity tomography techniques. In addition, cardiac dimensions, intramural deformations, and fiber shortening have been measured dynamically in the in situ canine heart throughout the cardiac cycle with implanted radiopaque markers and biplane roentgen techniques. Results of regional contraction and relaxation patterns are presented. Epicardial fiber shortening between apex and base were computed and found to be dependent on the duration of the preceding RR interval.

Animals↗