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PubMed2001

[Phase structure of the ejection period in the human cardiac function before and after 3-day water immersion].

Impedance cardiography was applied to 15 normal male volunteers before and after 3-d water immersion. Determined were parameters of central circulation and dependence of the ejection period on length of the cardiac cycle. Though the ejection period over the whole range of cardiac cycle lengths was shorter than "due" values determined as pre-immersion baseline, cardiac output after immersion was equal to and even slightly above baseline value. According to experimental results, this seems to be linked with little if any dependence of the fast ejection phase, hemodynamically most effective, on heart rate and volume loading which remained same as in the baseline period during all post-immersion tests. In contrast, the reduced ejection period, a variable of the ventricular blood evacuation, is materially dependent on heart rate and volume loading predetermining at large absolute and relative shortening of the ejection period after immersion.

Circadian Rhythm↗
PubMed1985

[Effects of injectable calcium blockers on cardiac function and relaxation in left ventricular hypertrophy].

Nineteen patients with left ventricular hypertrophy were given intravenous calcium antagonists: 9 patients received intravenous verapamil (VPM IV) and 10 patients diltiazem (DTZ) by intracoronary and then intravenous injection. Systemic and pulmonary resistances, cardiac output, left ventricular and aortic pressures, isometric contractility, isometric relaxation and left ventricular compliance were studied in sinus rhythm, during atrial and then ventricular pacing at 120/min and finally after tachycardia before and after administration of calcium antagonists. Left ventriculography in the 30 degrees RAO projection in sinus rhythm was performed before and after injection of the calcium antagonists to study the variations in the end diastolic volume, mass and mass-volume ratio. Finally, frame by frame numerisation of the ventriculographies during systole and diastole helped evaluate variations in amplitude, time and velocity of fibre shortening or lengthening. The administration of the calcium antagonists did not have any significant effect on heart rate (-2.8 +/- 10 p. 100, NS) or indices of isometric contractility (delta Vmax + 4 +/- 43 p. 100, NS). Significant falls in systemic and pulmonary resistances (-15 +/- 23 p. 100, p less than 0.05 and - 26 +/- 32 p. 100, p less than 0.05, respectively) and an increase in systolic index (+ 15.5 p. 100 +/- 12 p. 100, p less than 0.01) were observed. The improvement in left ventricular ejection was independent of the variation in resistances but was closely related to variations of parameters of relaxation. The effects on volumic compliance and filling velocities were also closely related to variations in relaxation (p less than 0.05 and p less than 0.01). Calcium antagonists protected left ventricular ejection during supraventricular tachycardia and prevented the changes in left ventricular relaxation observed during arrhythmias and after tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Influence of left ventricular mass regression on cardiac function in hypertensive elderly individuals.

A randomized, double-blind placebo controlled trial was conducted to compare the ability of verapamil and atenolol to induce regression of left ventricular mass in elderly hypertensive patients and the effects of regression on left ventricular filling, ejection fraction, and cardiac volumes. Forty-two individuals over 60 years of age were enrolled in the protocol. Eight of 21 patients assigned to atenolol and 18 to 21 assigned to verapamil achieved blood pressure control with single-agent therapy (p less than 0.05). The addition of chlorthalidone resulted in blood pressure control in the three remaining assigned to verapamil and in ten of the remaining patients assigned to atenolol. In the verapamil group left ventricular mass index decreased from 104 +/- 5 to 85 +/- 5 g/M2, while it was unchanged in the atenolol patients (109 +/- 9 to 112 +/- 10 g/M2). In the patients in whom the left ventricular mass regressed, the peak filling rate increased from 2.42 +/- 0.2 to 3.31 +/- 0.4 EDV/s, while it did not change in the patients who did not experience regression. Furthermore, ejection fraction and cardiac output were maintained in patients who had regression, both at rest and during mild upright bicycle exercise.

Aged↗
PubMed2000

L-arginine during long-term ischemia: effects on cardiac function, energetic metabolism and endothelial damage.

BACKGROUND: We have evaluated the addition of L-arginine, a precursor of nitric oxide, to a cardioplegic solution (named CRMBM) designed for long-term heart preservation. METHODS: Isolated isovolumic-perfused rat hearts (n = 22) were arrested with the CRMBM solution either with (Arg) or without L-arginine (2 mmol/L) (Arg group, n = 12, vs control group n = 10), submitted to 8 hours of cold storage (4 degrees C) in the solution, and then reperfused for 60 minutes at 37 degrees C. In 11 hearts, we evaluated the quality of cardiac preservation with P-31 magnetic resonance spectroscopy and the measure of function and cellular integrity. Endothelium-dependent and independent vasodilatations were measured in 11 other hearts, using 5-hydroxytryptamine and papaverine to assess endothelial and smooth muscle function. RESULTS: Adding L-arginine to the cardioplegic solution improved functional recovery during reflow, as shown by the rate pressure product (31% +/- 3% for control vs 47% +/- 3% for Arg, p = 0.003) together with higher coronary flow and diminished contracture. Purine release in coronary effluents during reperfusion was lower in the Arg group. During ischemia and reflow kinetics of intracellular pH and high-energy phosphates were similar in both groups. Coronary endothelium-dependent vasodilatation was similarly impaired in both groups, but smooth muscle was less altered with L-arginine. CONCLUSIONS: As an additive to the CRMBM cardioplegic solution, L-arginine provides a protective effect for long-term heart preservation. Our data do not show coronary endothelial protection as the prominent mechanism.

Animals↗
PubMed1992

The cardiac functional reserve in elderly hypertensive patients with abnormal diurnal change in blood pressure.

OBJECTIVE: To evaluate the left ventricular function of hypertensive patients with abnormal diurnal change in blood pressure. DESIGN: We compared left ventricular structural and functional characteristics between hypertensive patients with a normal diurnal change in blood pressure (H2 group) and those with a nocturnal blood pressure increment (H1 group) using echocardiography. METHODS: The study group consisted of 36 hypertensives and 16 normotensives whose 24-h ambulatory blood pressure monitorings were measured non-invasively. The hypertensive group was subdivided into the H1 group, consisting of 11 patients (76 +/- 7 years), and the H2 group with 25 patients (73 +/- 7 years). The normotensive control group had a mean age of 73 +/- 6 years. Echocardiographic examinations were performed before and at the end of isometric exercise (handgrip for 3 min) and isoproterenol infusion (0.02 micrograms/kg per min for 5 min). RESULTS: The left ventricular mass index in the H1 group was significantly greater than in the H2 or control group. Left ventricular fractional shortening (LVFS) at rest in the H1 group was also significantly greater than in the other two groups. However, the peak late: early diastolic filling ratio, which indicated diastolic function, significantly deteriorated in the H1 group compared with the H2 and control groups. Furthermore, changes in LVFS after isometric exercise in the H1 group were more suppressed than in the H2 or control group. In addition, a significantly lower increment in LVFS after isoproterenol was observed in the H1 group compared with the H2 or control group. CONCLUSION: The H1 group had greater left ventricular mass and impaired left ventricular functional reserve than the H2 group.

Aged↗
PubMed1981

Effects of antidepressants on cardiac function.

Most antidepressants may affect the cardiovascular system adversely although their mode of action in causing these complications differs. They affect the cardiovascular system directly or through drug interactions. They may affect blood pressure, the inotropic state of the heart and cardiac conduction. The causes of these complications are discussed with relevance to the known action of these agents. Although serious cardiovascular complications do not occur frequently at therapeutic dosage, a knowledge of these abnormalities is essential for safe prescribing. After overdose many of these agents may prove lethal.

Antidepressive Agents↗
PubMed1991

Cardiac function of the diabetic renovascular hypertensive rat: effects of insulin and thyroid hormone treatment.

The influences of hypertension and hypothyroidism on diabetic cardiomyopathy are not clear. We studied this problem further by characterizing the effects of chronic triiodothyronine (T3) treatment on cardiac performance of diabetic renovascular hypertensive (RVH) rats. Hypertension was effected by clipping the left renal artery of Wistar-Kyoto (WKY) rats, and diabetes was induced 2 weeks later by streptozotocin (STZ; 55 mg/kg i.v.). The WKY strain was selected because it is relatively resistant to the cardiodepressant effects of diabetes, so that the influence of superimposed hypertension would be more apparent. Performance of working Krebs-Henseleit buffer perfused hearts was quantified by measuring left ventricular pressure and flow characteristics. The results showed that renovascular clipping caused a marked hypertension and left ventricular hypertrophy (LVH) but had no effect on perfused heart performance after 10 weeks. They also showed that diabetes during the final 8 weeks (i) caused a marked impairment in the performance of perfused hearts ex vivo of hypertensive rats but had no measurable effect in the normotensive WKY, (ii) had no effect on arterial pressure of either the normotensive or the hypertensive rats but reduced heart rate of hypertensive animals in vivo, and (iii) caused equivalent hyperglycemia, hypoinsulinemia, and hypothyroidism (depressed serum T3 and T4 levels) of hypertensive and normotensive rats. Treatment of diabetic RVH rats with T3 (10 micrograms.kg-1.day-1) in vivo was nearly as effective as insulin therapy (10 U.kg-1.day-1) in preventing the cardiac dysfunction ex vivo and was as effective as insulin therapy in preventing the bradycardia in vivo and the decline loss.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

The role of nuclear cardiology procedures in the evaluation of cardiac function following heart transplantation.

Heart transplantation is, today, an accepted and recommended modality in the management of selected patients suffering from terminal heart disease. However, acute rejection and infection remain the major complications of this operation. Serial endomyocardial biopsy (EB), considered as the standard for diagnosis of cardiac rejection, is an invasive and delicate operation, not free of complications, even when done by skilled personnel in specialized centers. The object of this study was to compare and correlate between radionuclide ventriculography (RNV) and the histologic findings of EB. Furthermore, to validate the use of nuclear cardiology techniques that allow noninvasive, reliable, and rapid quantitation of ventricular function and myocardial perfusion for the diagnosis and management of rejection in patients with heart transplants. Radionuclide studies of left ventricular function were performed in 3 heterotopic heart transplant patients (HHT) with long term survival and early after the operation in 5 patients with HHT, 12 orthotopic heart transplants (OHT) and in 2 heart and lung transplants (HLT). Simultaneous EBs were performed in the early posttransplant patients and a histologic score for acute rejection was obtained. First pass (FP) and multigated equilibrium blood pool ventriculography, using the in vivo 99mTc-labelling of RBCs was used to measure left ventricular volumes (LVV) such as stroke volume (SV), end-diastolic volume (EDV), end-systolic volume (ESV), and both global and regional ejection fraction (EF, REF). The histological grading of acute rejection was classified into four groups: (1) no rejection, (2) mild rejection, (3) moderate rejection, and (4) severe rejection. The median of each LVV parameter was calculated and correlated with the EB using a nonparametric one way analysis of variance. A percentage change of LVVs was used rather than the difference of the calculated LVVs. During moderate acute rejection, SV had the highest correlation in P less than 0.004, followed by the EDV (P less than 0.05), and finally ESV (P less than 0.02). During severe acute rejection the correlation was SV (P less than 0.0008), EDV (P less than 0.001), and ESV (P less than 0.006). Myocardial perfusion scintigraphy using 201T1 was performed in the HHT patients, although, at this stage we have not attempted a correlation with the histologic findings. In one patient with long term survival OHT, increased 131I-metaiodobenzylguanidine (MIBG) myocardial uptake was evident during a rejection episode.

Adolescent↗
PubMed2005

Angiotensin AT2 receptor deficiency after myocardial infarction: its effects on cardiac function and fibrosis depend on the stimulus.

Hearts of normotensive angiotensin II type 2 receptor (AT2)-deficient mice do not develop fibrosis after angiotensin II-induced chronic hypertension. Thus, the goal of our study was to clarify whether AT2 knockouts (KOs) are also characterized by altered left ventricular (LV) function and modified remodeling of the extracellular matrix (ECM) after induction of myocardial infarction (MI). MI was induced in 5-mo-old female AT2-deficient mice and controls by occlusion of the left coronary artery. Time-matched sham-operated animals served as controls. After 48 h, the first sets of mice were hemodynamically characterized using a pressure-tip catheter (n = 8/group). We also obtained pressure volume loops using a microconductance catheter in additional sets of animals 3 wk after induction of MI (n = 7/group). Finally, the collagen index was illustrated by Sirius red staining and quantified by digital analysis. Whereas the LV function of sham-operated animals did not differ between both genotypes, the collagen index was 44% lower in KO animals. Forty-eight hours and 3 wk post-MI, systolic and diastolic LV function were impaired in both AT2-deficient and wild-type (WT) animals to the same extent by approx 45%. No differences were found between the two genotypes with respect to LV hypertrophy and the fibrosis index in the infarcted and noninfarcted areas 3 wk post-MI. While AT2-KO mice had less cardiac collagen content under basal conditions, the receptor deficiency had no significant influence on LV function at the two investigated time points after induction of MI or on the remodeling of ECM at the latter time point. Thus, hypertension-induced fibrosis is probably triggered by other control mechanisms than fibrosis induced by MI.

Animals↗
PubMed1993

[Effects of urapidil by intravenous injection on pulmonary circulation and cardiac function in left ventricular failure].

The hemodynamic effects of urapidil were studied in 10 patients with secondary pulmonary hypertension investigated for the purpose of possible inclusion on a heart transplant waiting list. All patients gave their consent to participate. Nine patients had a dilated cardiomyopathy and 1 three-vessel coronary disease with diffuse hypokinesia. All were treated with digitalis, diuretics, converting enzyme inhibitors or calcium antagonists. Hemodynamic effects were measured 5 and 25 minutes after the slow intravenous injection of 50 mg of urapidil. Urapidil caused a significant decrease in pulmonary pressures (-20%) and total pulmonary resistance (-42.5%). The fall in systemic arterial resistance was of the same degree (41.5%). The fall in pulmonary arterial resistance was also significant (-26%). The increase in cardiac output was +35%, with no change in left ventricular myocardial function indices. Thus, in patients with congestive left ventricular failure and secondary pulmonary hypertension already treated with vasodilators, urapidil resulted in a hemodynamic improvement after intravenous administration, demonstrating a synergistic action with that of other vasodilators. This synergistic action could be used to test pulmonary arteriolar vasodilatation reserves during the hemodynamic assessment of patients in whom a heart transplant is contemplated.

Antihypertensive Agents↗
PubMed1986

Long-term follow-up of cardiac function in patients with Hodgkin's disease treated with mediastinal irradiation and combination chemotherapy including doxorubicin.

Among 41 evaluable patients whose first treatment for advanced Hodgkin's disease had consisted of alternating cycles of mechlorethamine, vincristine, prednisone, and procarbazine (MOPP), and doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD), in addition to low-dose mediastinal irradiation, 19 underwent retrospective cardiac evaluation by routine posteroanterior and lateral chest x-ray, 12-lead ECG, M-mode echocardiogram, and ECG-gated left ventricular blood pool scan at rest and during exercise. Fifteen patients had unequivocally normal left ventricular function by all these parameters. Two patients had minimally reduced left ventricular ejection fraction (LVEF) at rest with a normal increment with exercise. In two other patients with high normal resting LVEF and subnormal increment with exercise, the elevated resting values implied initial measurement in a nonbasal state. A twentieth patient (the oldest; one of two with active Hodgkin's disease at the time of evaluation and the stimulus for this study) had markedly reduced LVEF as determined by radionuclide cardiac angiography and had developed clinical congestive heart failure shortly before evaluation. Despite this patient, the study indicates that treatment with MOPP/ABVD and low-dose mediastinal irradiation entails low risk for cardiac complications.

Adult↗