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17 patients were treated by atrial (AAI) or atrial-triggered ventricular pacing (VAT). The atrial electrode was placed using a new endocardial screw-in technique. No complications occurred during a follow-up period of 3 months. Cardiac output at rest was measured in 12 patients before pacemaker implantation and was 3.571/min with VVI pacing at a heart rate (HR) of 70/min and 3.97 l/min (HR 75/min) with AAI or VAT pacing (p less than 0.001). Measurement of cardiac output was repeated in 7 patients with AV-block III degrees 10 weeks after pacemaker implant and the result was 4.40 l/min (HR 77/min) on VAT stimulation. During dynamic exercise in 5 patients, cardiac output under VAT pacing was 20% higher than with VVI pacing. This difference remained unchanged after 10 weeks. It is concluded that atrial electrodes can be placed reliably by the new technique. In contrast to VVI pacing, the hemodynamic benefits of atrial-triggered ventricular pacemakers appear to be long lasting.
LV wall motion from monoplan, RAO projected LV angiograms is one of the most important parameters for LV function studies. Different methods to describe wall motion are reported in the lit., including procedures to correct distortions from x-ray techniques. With physiological contraction patterns as the basis a method is described, in which systolic contraction is performed radially with its center being the mean point of the diastolic long axis of the projected LV area. Wall motion was measured at 20 degrees distances circular around mean point, starting from the aorta. The mean deviation of the systolic long axis frm diastolic one was 8.5 degrees. This angle was corrected. The comparison of this procedure with six other methods reported in the lit. shows, that there are differences in wall motion up to 100%, depending on the model used. We conclude, that a standardized procedure to measure wall motion is necessary, which is described here.
A complex of examinations (ECG, echocardiographic and X-ray evaluations of heart volumes and cavities, treadmill-test) was performed in 82 patients before and after reoperations on the mitral valve. The type of recorrection was found to be associated with the degree of positive dynamics of the results. The data obtained contradicted to hyperdiagnoses of primary medical-labor examination commission establishing the II group of invalidism in 86 +/- 4% (M +/- m) of the examined patients. As a result of an analysis of all the data obtained the number of such patients was reduced up to 34 +/- 5%. A new approach to solving the problem of medical-labor examination was shown to be necessary for patients reoperated for mitral disease of the heart.
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The aim of this prospective study was to confirm whether and when a fall in gas transfer occurs following heart transplantation (HT); and to examine the potential relationship between gas transfer and haemodynamic change, immuno-suppression and cytomegalovirus (CMV) infection. The lung physiology of 34 heart transplant recipients (HTR) and 14 control patients undergoing coronary artery bypass grafting (CABG) were studied. The absolute and standardized residual values of forced expiratory volume in one second (FEV1), forced vital capacity (FVC), residual volume (RV), forced residual volume (FRC), total lung capacity (TLC), transfer factor of the lungs for carbon monoxide (TL,CO) and carbon monoxide transfer coefficient (KCO) were measured before and at 30, 60, 90, 120 and 150 days after HT. These data were compared to haemodynamic status, graft rejection, cyclosporin levels and episodes of CMV infection. Lung function was studied in a group of patients before and 4 weeks after CABG. There was a significant fall in mean KCO after HT (pre-HT = 1.29 and post-HT = 1.06 mmol.min-1.kPa.L-1) but not after CABG (pre-CABG = 1.49, post-CABG = 1.5 mmol.min-1.kPa.L-1. No relationship was observed between gas transfer and CMV. At the latest stage following HT (150 days) there was a positive correlation between TL,CO (absolute value and standardized residual) and mean cyclosporin level (r = 0.48 and r = 0.44, respectively) and also between the absolute KCO and actual (r = 0.56) and mean (r = 0.55) cyclosporin levels. Following HT, there is an early fall in gas transfer, which is independent of the effects of surgery and bypass, implicating early immunosuppression (e.g. antithymocyte globulin/cyclosporin).
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To estimate the pumping function of the left-sided heart in patients with "latent" left-sided heart failure due to heart disease which primarily affected the left-side of the heart (former NYHA class I and II), we measured (i) the increase of peripheral venous pressure in response to supine mild leg exercise (delta VP), and (ii) the increase of plasma noradrenaline (NA) concentration due to phentolamine (PH) injection (delta NAPH). We divided the patients into well-functioning left-sided heart group (delta CI/delta PAW greater than 0.180 L.min-1.M-2.mmHg-1) and poorly-functioning left-sided heart group (delta CI/delta PAW less than or equal to 0.180 L.min-1.M-2.mmHg-1) on the basis of a ratio (delta CI/delta PAW), relating the increase in cardiac index (delta CI) in response to exercise to the concomitant increase in mean pulmonary artery wedge pressure (delta PAW). This diving line (delta CI/delta PAW = 0.180 L.min-1.M-2.mmHg-1) correlated with delta VP (diving line: delta VP = 35 mmH2O) and with delta NAPH (diving line: delta NAPH = 0.353 ng/ml). Our results suggest that delta VP and delta NAPH reflected the pumping function of the left-sided heart with considerable accuracy.
Patients in congestive heart failure are known to have altered autonomic responses to circulatory stress. In this study, two different age groups of male coronary heart disease (CHD) patients, not in failure, as well as normal male subjects, underwent standard 20-min 70 degrees head-up tilt and Valsalva tests. Responses were monitored by noninvasive methods and cardiac output was estamated with a transthoracic impedance method. During tilt, the CHD patients and control subjects had similar heart rate and diastolic pressure responses. However, the CHD patients had a greater decline in pulse pressure during tilt, mainly due to a decrease in systolic pressure. CHD patients had lesser declines in stroke volume and cardiac index and lesser increases in total vascular resistance than did control subjects. In the Valsalva, the heart rate phase increments (and decrements) from control and rate increments (and decrements) between successive phases were less in the coronary patients. The results indicate that coronary patients, not in failure, have diminished circulatory responses to the tilt and Valsalva maneuver and suggest that these tests may be useful functional indices of cardiovascular capability in coronary disease.
12 patients with the diagnosis of coronary heart disease and angina pectoris underwent evaluation of heart rate as an indicator of tolerance of a given work load. A floating catheter in a pulmonary artery and a peripheral arterial catheter permitted measurement of blood pressures. Oxygen uptake per minute (VO2) was measured by Douglas bags and oxygen content of arterial and mixed-venous blood was determined at rest and during each minute of submaximal and symptom-limited maximal exercise on a treadmill. In the minute of exercise, in which 60-80% (mean 71.3%) of maximal heart rate (HF max) were attained, VO2 averaged 60.3% VO2 max, cardiac output (Q) 72.5% Q max and mean pulmonary arterial pressure (PAP) 26.6 mm Hg. With one exception, Q leveled off or dropped in the last minutes of exercise beyond 85% HF max. Heart rate (HF), oxygen difference between arterial and mixed venous blood (DavO2) and PAP reached their highest values in the last minute. It is suggested that heart rates up to 70% HF max, as individually determined in a symptom-limited maximal exercise test, are the tolerable limit during occupational activities. 85% HF max should not be exceeded during exercise training. Left ventricular function may be impaired beyond that limit because of acute coronary or myocardial insufficiency, and the regulation of cardiac output becomes uneconomical.
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Although in physiology the heart is often referred to as a simple piston pump, there are in fact two additional features that are integral to cardiac physiology and function. First, the heart as it contracts in systole, also rotates and produces torsion due to the structure of the myocardium. Second, the heart produces a significant electromagnetic field with each contraction due to the coordinated depolarization of myocytes producing a current flow. Unlike the electrocardiogram, the magnetic field is not limited to volume conduction and extends outside the body. The therapeutic potential for interaction of this cardioelectromagnetic field both within and outside the body is largely unexplored. It is our hypothesis that the heart functions as a generator of bioinformation that is central to normative functioning of body. The source of this bioinformation is based on: (1) vortex blood flow in the left ventricle; (2) a cardiac electromagnetic field and both; (3) heart sounds; and (4) pulse pressure which produce frequency and amplitude information. Thus, there is a multidimensional role for the heart in physiology and biopsychosocial dynamics. Recognition of these cardiac properties may result in significant implications for new therapies for cardiovascular disease based on increasing cardiac energy efficiency (coherence) and bioinformation from the cardioelectromagnetic field. Research studies to test this hypothesis are suggested.