[Changes in diastolic left ventricular function in hypertension with left atrial enlargement].
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Left ventricular function in mitral regurgitation has typically been studied in models that either sever the chordae tendineae or create a ventriculoatrial shunt. These methods may have adverse effects on left ventricular function independent of the regurgitant lesion. An animal model of chronic mitral regurgitation was therefore developed that both preserves annuloventricular continuity and avoids the use of external shunts. A circular 0.16 to 0.24 mm/kg defect was created in the anterior mitral valve leaflet of weanling sheep under direct vision with the aid of cardiopulmonary bypass. Six animals were studied preoperatively and immediately postoperatively (acute regurgitation group), and 20 animals were studied 8.1 +/- 0.2 (mean +/- one standard deviation) months postoperatively (chronic regurgitation group). Animals with chronic mitral regurgitation were compared with an age- and weight-matched control group that was not operated on (n = 7). Volumetric data and ejection fraction were derived from digitalized cineangiographic images. Maximal elastance was calculated from pressure-volume loops obtained from the simultaneous recording of left ventricular pressure by micromanometer-tipped left ventricular catheters, and volumes were obtained from digitalized images of epicardial echocardiographic recordings. Mitral valve perforation resulted in 3+ to 4+ mitral regurgitation and a calculated regurgitant fraction of 37% +/- 7% (mean +/- one standard deviation). Acute mitral regurgitation was associated with an increase in left ventricular end-diastolic volume from 110 +/- 17 to 121 +/- 23 ml (p < or = 0.05) and no change in end-systolic volume. These changes were associated with an increase in fractional shortening, from 29% +/- 11% to 40% +/- 10% (p < or = 0.05), and an increase in velocity of circumferential shortening, from 1.5 +/- 0.7 to 2.9 +/- 0.7 circ/sec (p < or = 0.05). However, there was no change in maximal elastance, a load-independent index of left ventricular function. Conversely, animals with chronic mitral regurgitation exhibited an elevated end-diastolic volume (202 +/- 32 versus 145 +/- 34, p < or = 0.05), an elevated end-systolic volume (104 +/- 17 versus 63 +/- 20 ml, p < or = 0.05), and a reduced ejection fraction (48% +/- 6% versus 57% +/- 9%, p < or = 0.05) compared with controls.(ABSTRACT TRUNCATED AT 400 WORDS)
CONTEXT: Exercise training in patients with chronic heart failure improves work capacity by enhancing endothelial function and skeletal muscle aerobic metabolism, but effects on central hemodynamic function are not well established. OBJECTIVE: To evaluate the effects of exercise training on left ventricular (LV) function and hemodynamic response to exercise in patients with stable chronic heart failure. DESIGN: Prospective randomized trial conducted in 1994-1999. SETTING: University department of cardiology/outpatient clinic in Germany. PATIENTS: Consecutive sample of 73 men aged 70 years or younger with chronic heart failure (with LV ejection fraction of approximately 0.27). INTERVENTION: Patients were randomly assigned to 2 weeks of in-hospital ergometer exercise for 10 minutes 4 to 6 times per day, followed by 6 months of home-based ergometer exercise training for 20 minutes per day at 70% of peak oxygen uptake (n=36) or to no intervention (control group; n=37). MAIN OUTCOME MEASURES: Ergospirometry with measurement of central hemodynamics by thermodilution at rest and during exercise; echocardiographic determination of LV diameters and volumes, at baseline and 6-month follow-up, for the exercise training vs control groups. RESULTS: After 6 months, patients in the exercise training group had statistically significant improvements compared with controls in New York Heart Association functional class, maximal ventilation, exercise time, and exercise capacity as well as decreased resting heart rate and increased stroke volume at rest. In the exercise training group, an increase from baseline to 6-month follow-up was observed in mean (SD) resting LV ejection fraction (0.30 [0.08] vs 0.35 [0.09]; P=.003). Mean (SD) total peripheral resistance (TPR) during peak exercise was reduced by 157 (306) dyne/s/cm(-5) in the exercise training group vs an increase of 43 (148) dyne/s/cm(-5) in the control group (P=.003), with a concomitant increase in mean (SD) stroke volume of 14 (22) mL vs 1 (19) mL in the control group (P=.03). There was a small but significant reduction in mean (SD) LV end diastolic diameter of 4 (6) mm vs an increase of 1 (4) mm in the control group (P<.001). Changes from baseline in resting TPR for both groups were correlated with changes in stroke volume (r=-0.76; P<.001) and in LV end diastolic diameter (r=0.45; P<.001). CONCLUSIONS: In patients with stable chronic heart failure, exercise training is associated with reduction of peripheral resistance and results in small but significant improvements in stroke volume and reduction in cardiomegaly. JAMA. 2000.
BACKGROUND: Assessment of left ventricular function by echocardiography is frequently challenging in mechanically ventilated patients. We evaluated the potential value of contrast-enhanced imaging and tissue harmonic imaging over standard fundamental imaging for endocardial border detection (EBD) in these patients. METHODS AND RESULTS: Fifty patients underwent standard transthoracic 2D echocardiography and were imaged in fundamental and tissue harmonic modes and subsequently with intravenous contrast (Optison). Two echocardiographers reviewed all studies for ease of visualization of endocardial border segments and scoring of wall motion. EBD for each wall segment was graded from 1 to 4 (1 = excellent EBD). Wall motion was scored by a standard 16-segment model and 1 to 5 scale. Studies were categorized as nondiagnostic if 4 of 6 segments in the apical 4-chamber view were either poorly seen or not seen (EBD score 3 or 4). Quantification of ejection fraction was independently performed offline. Visualization of 68% of all segments improved with contrast echocardiography versus 17% improvement with tissue harmonics compared with fundamental mode. Significant improvement (poor/not seen to good/excellent) occurred in 60% of segments with contrast echocardiography versus 18% with tissue harmonics. A total of 850 segments were deemed poor/not seen, 78% of which improved to good/excellent with contrast echocardiography versus 23% with tissue harmonics. Interobserver agreement on EBD was 64% to 70%. Conversion of nondiagnostic to diagnostic studies occurred in 85% of patients with contrast echocardiography versus 15% of patients with tissue harmonics. Scoring of wall motion with fundamental mode, tissue harmonics, and contrast echocardiography was possible in 61%, 74%, and 95% of individual segments, respectively (P <.001). Wall motion scoring was altered in 17% of segments with contrast echocardiography and in 8% with tissue harmonics. Interobserver agreement on wall motion scoring was 84% to 88%. Contrast echocardiography permitted measurement of ejection fraction 45% (P =.003) more often over fundamental mode versus a 27% (P =.09) increase with tissue harmonics. CONCLUSIONS: Contrast echocardiography is superior to tissue harmonic imaging for EBD, wall motion scoring, and quantification of ejection fraction in mechanically ventilated patients.
The widely accepted theories for the decreased function in the stunned myocardium relate to Ca2+ desensitization and free radical-mediated tissue damage of the myofilaments. The aim of the present study was to examine whether the depressed contractile function and Ca2+ responsiveness of the stunned myocardium may be restored by a new Ca2+ sensitizer (levosimendan), which has been shown to improve the Ca2+ response of the myofilaments. The effects of levosimendan on the left ventricular function and the in vivo protein phosphorylation were examined in both the non-ischemic and the stunned myocardium. Myocardial stunning was induced in Langendorff-perfused guinea pig hearts by suspending the circulation for 8 min, followed by a 20-min reperfusion period. Perfusion of post-ischemic guinea pig hearts with levosimendan (0.03-0.48 microM, 6 min) was associated with dose- and time-dependent increases in both dP/dtmax (contractility) and dP/dtmin (speed of relaxation). When the effectiveness of levosimendan was compared in non-ischemic and post-ischemic hearts, no significant differences were noted in the relative stimulatory effects on contractility and relaxation, at any given time point (time-response curve) or concentration (dose-response curve). Perfusion of the guinea pig hearts with a high (0.3 microM) levosimendan concentration did not reveal any qualitative or quantitative difference in the phosphodiesterase inhibitory potential of the compound (elevation of tissue cyclic AMP levels and characteristics of protein phosphorylation) between the non-ischemic and the post-ischemic myocardium. However, when isoproterenol was administered to induce maximal in vivo phosphorylation of cardiac phosphoproteins, an attenuation of the 32P-incorporation into troponin I was noted in the post-ischemic hearts. The decrease in isoproterenol-induced 32P-incorporation into troponin I was associated with similar alterations in the tissue level of this protein. We conclude that the Ca2+ sensitizer levosimendan exerts dose- and time-dependent positive inotropic and lusitropic effects on the post-ischemic myocardium, lending support to the hypothesis tha Ca2+ desensitization of the myofibrils is involved in myocardial stunning.
Surgery for degenerative mitral regurgitation has become complex. Preservation of annulo-ventricular continuity through the chordae tendineae is an important determinant of operative survival, postoperative left ventricular function, long-term survival, and quality of life. Some cardiologists believe that NYHA I function is never achieved after conventional mitral replacement with chordal transection. Valve repair is the procedure of choice but when valve replacement is inevitable every effort should be made to preserve the posterior leaflet and its chordal attachments. Valve replacement with preservation of the subvalvar apparatus provides a functional outcome similar to that after valve repair but usually leads to life long anti-coagulation.
The left ventricular function of 26 workers exposed to fluorine was investigated. The results demonstrated that the LVET in the higher urine fluorine group (greater than 1.5 mg/L) was significantly shorter than the control group (P less than 0.01), the PEP was much longer than the control group (P less than 0.05), and the rate of PEP/LVET compared with the control group was increased. The difference was statistically significant (P less than 0.01). In the lower urine fluorine group (less than 1.5 mg/L) the time of LVET and PEP and the rate of PEP/LVET was not significantly different from the control group. The results showed that excessive fluorine ion in the body could cause decrease of myocardial contraction. The reason may be, that the fluorine ion inhibits the activities of certain enzymes in the body, thereby producing inhibition of ATP supply and utilization.
The left ventricular function was assessed in 70 diabetics under 60 years of age without clinically evident heart disease using established non-invasive methods, these include systolic time interval method and echocardiography. The ratio of pre-ejection period to left ventricular ejection time (PEP/ET) was remarkably elevated in diabetics with severe microangiopathy (0.431 +/- 0.037). Even in diabetics without microangiopathy PEP/ET ratio was significantly higher (0.374 +/- 0.037) compared with that in controls (0.331 +/- 0.023, P less than 0.01). Most of diabetics with a PEP/ET value of higher than 0.40 were not under proper care with regard to diabetic control. A tendency toward normalization of PEP/ET values was often observed with the improvement in diabetic control during six to twelve months among the inadequately controlled diabetics. Isovolumic relaxation time in diabetics was longer than in controls (80 +/- 14 msec, 59 +/- 11 msec, P less than 0.005). Our results suggest that abnormalities of left ventricular function in diabetics may be related to not only severity of microangiopathy but also the state of diabetic control. The maintenance of adequate control of diabetes seems to play an important role in the prevention of congestive heart failure in patients with diabetes mellitus.
To determine the relationship of left ventricular function and ventricular tachycardia, 48 hour ECG monitoring and technetium-99m gated equilibrium radionuclide angiography were performed in 84 consecutive patients with hypertrophic cardiomyopathy and sinus rhythm. Measurements of ejection fraction (EF), peak ejection rate (PER, edv/s), peak filling rate (PFR, edv/s) and time to peak filling rate (PFR, ms) were derived from radionuclide activity time curves generated from data acquired in list-mode. Left ventricular function was compared in patients with and without ventricular tachycardia. Left ventricular ejection fraction was significantly lower in 16 patients with ventricular tachycardia compared to 68 patients without (67 +/- 17 vs 78 +/- 10, P less than 0.05) and time to peak filling rate was significantly prolonged (152 +/- 32 vs 120 +/- 36, P less than 0.05). Thus patients with hypertrophic cardiomyopathy at greatest risk of sudden death had significant impairment of systolic and diastolic left ventricular function.
The interrelations between physical working capacity and left ventricular function were studied in 51 patients with mitral valvular disease (17 men and 34 women) by impedance cardiography. A number of physical working capacity indices and the impedanve cardiographic indices of the ejection and contractile functions of the left ventricle were determined. As an approximate assessment of the left ventricular function the degree of the changes of the impedance cardiographic indices from the state of rest to physical loading was used. A better correlation was established between the physical working capacity and the increase if the impedance cardiographic indices of the ejection and contractile left ventricular functions from the state of rest to physical loading than with the same indices determined in the state of rest only. The impedance cardiographic indices of the left ventricular function by physical loading increase to a lesser degree in patients with diminished left ventricular function at rest (combined mitral valvular disease) while in the patients with normal left ventricular function at rest ("pure" mitral stenosis) the changes are like those in healthy persons.
BACKGROUND: Left ventricular function after acute myocardial infarction (AMI) is determined by the expansion of the infarct zone and remodeling of the noninfarcted myocardium. An occluded infarct-related artery (IRA) is an independent risk factor for remodeling. METHODS AND RESULTS: Changes in myocardial collagen metabolism were evaluated in 36 patients with suspected AMI. The plasma creatine kinase MB fraction and myoglobin release curves were analyzed for assessment of early reperfusion and infarct size. Collagen scar formation was evaluated by measurement of serum concentrations of the aminoterminal propeptide of type III procollagen (PIIINP), the aminoterminal propeptide of type I procollagen (intact PINP), and the carboxyterminal propeptide of type I procollagen (PICP). Plasma renin activity and urine excretion of cortisol and aldosterone were also measured. Coronary angiography and left ventricular cineangiography were performed during early hospitalization. The serum concentration of PIIINP increased from 3.50+/-0.20 to a maximum of 5.08+/-0.36 microg/L (n=32) in the patients with AMI, whereas the concentrations of intact PINP and PICP tended to decrease. The area under the curve (AUC) of PIIINP during the first 10 postinfarction days was larger in patients with severe heart failure or ejection fractions < or = 40% than in those with no heart failure or with an ejection fraction > 40% (P<.05 and P<.01, respectively), and it was also larger in the patients with TIMI grade 0 to 2 flows than in those with TIMI 3 flows (P<.05), despite similar enzymatically determined infarct sizes. No significant correlations between PIIINP and neurohumoral parameters were observed. The AUC of PIIINP and the change in PIIINP during the first 4 days were significantly correlated with indices of cardiac function. CONCLUSIONS: Collagen scar formation after AMI can be quantified by measurement of serum PIIINP concentrations. Scar formation is more prominent in large infarctions causing left ventricular dysfunction and in patients with occluded IRAs.
The left ventricular function during ramp exercise was assessed using 99mTc-labeled red blood cells and a Wireless Telemetric Cardiac Monitoring System (WTCMS) in 34 patients who received coronary angiography. Sequential changes in the left ventricular ejection fraction (EF) during exercise, were classified into the two types, normal response (up slope pattern) and abnormal response (horizontal, down slope and up-down slope pattern) when defined the response as 5 percent or more increment of EF as normal. Six patients without significant stenosis by coronary angiography showed normal response. Seventeen of 28 patients with coronary disease showed abnormal response (sensitivity 61%). Eight of 11 patients (73%) with coronary disease and normal response showed no redistribution on the stress thallium myocardial scintigraphy. Twelve of 17 patients (71%) with coronary disease and abnormal response showed redistribution by the stress thallium scintigraphy. Horizontal and down slope patterns of EF during exercise were more often noted in the groups with redistribution and multivessel coronary disease. After the exercise, the times to the over shoot was significantly longer in groups with redistribution (p < 0.01) in comparison with groups without redistribution. From these results, we conclude that the monitoring the changes in left ventricular activity during ramp exercise with the WTCMS is a very useful method for the evaluation of the sequential changes in left ventricular function in patients with ischemic heart disease.
To determine the effect of coronary disease progression on left ventricular function, 47 patients who had two cardiac catheterizations at a mean interval of 25 months (range three to 92 months) without intervening surgery were studied. Of these, 35 patients had coronary disease and 12 patients had normal or near normal coronary arteries. Coronary disease progression was seen more often in patients with initial coronary disease than in those without significant disease (66 percent vs 25 percent, p less than 0.02). Left ventricular ejection fraction decreased in patients with coronary disease progression (0.63 +/- 0.03 to 0.51 +/- 0.04, p less than 0.01) but was unchanged in patients without progressive disease (0.58 +/- 0.04 to 0.57 +/- 0.93, p = NS). Interval myocardial infarction was the major cause of deteriorating left ventricular function. The rate or degree of coronary disease progression did not predictably change global left ventricular function, and progressive disease in individual vessels did not predictably alter regional left ventricular function. The presence or development of collateral vessels did not significantly alter ventricular performance.
Propafenone is a class Ic anti-arrhythmic agent with mild beta-blocking properties which has recently become available in South Africa. We have used the drug in 3 patients with sustained monomorphic ventricular tachycardia not due to ischaemic heart disease. All had normal left ventricular function; 1 had Wegener's granulomatosis and 2 had arrhythmogenic right ventricular dysplasia. In the latter 2, propafenone provoked incessant monomorphic ventricular tachycardia which persisted for more than 24 hours despite repeated efforts at termination. The morphology was similar to the patients' spontaneous ventricular tachycardia, but the rate was slower and the QRS complexes broader, consistent with propafenone's marked ability to slow intraventricular conduction. It is postulated that incessant tachycardia results from perpetuation of re-entry due to marked conduction slowing produced by the drug. Previous reports have suggested that this is most likely to occur in patients with poor left ventricular function, but our experience indicates that those with normal left ventricular function are also at risk, particularly if the substrate for re-entry is present. Propafenone, like all other powerful anti-arrhythmic agents, may provoke life-threatening arrhythmias and should be used with great caution after due consideration of the indications, even in patients with normal left ventricular function.
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The action on left ventricular function of Astragalus Membranaceus (AM), a Qi-tonic, in 20 patients with angina pectoris was studied by means of Doppler Echocardiogram (DEC). It showed that cardiac output increased from 5.09 +/- 0.21 to 5.95 +/- 0.18 L/min 2 weeks after AM was administered (P < 0.01), and no improvement of left ventricular diastolic function appeared. Adenosine triphosphatase activity was not inhibited by using AM, which was different from that of digitalis.
UNLABELLED: 18F-FDG PET can identify areas of myocardial viability and necrosis and provide useful information on the effectiveness of experimental techniques designed to improve contractile function and myocardial vascularization in small animals. The left ventricular volume (LVV) and left ventricular ejection fraction (LVEF) in normal and diseased rats were measured in vivo using the high-resolution avalanche photodiode (APD) small-animal PET scanner of the Université de Sherbrooke. The measurements obtained by PET were compared with those obtained by high-resolution echocardiography and with known values obtained from a small, variable-volume cardiac phantom. METHODS: List-mode gated (18)F-FDG PET studies were performed using the APD PET scanner on 30 rats: 11 healthy, 4 under septic shock, and 15 with heart failure induced by ligature of the left coronary artery. PET images were resized to match human-scale pixels and analyzed using a standard clinical cardiac software program. The LVV and LVEF from the same animals were also evaluated by echocardiography. RESULTS: Agreement was excellent between the endocardial volumes determined by PET and the actual volumes of the cardiac phantom (r(2) = 0.96). Agreement between PET and echocardiography for LVV ranged from good in healthy rats (r(2) = 0.89) to fair in diseased rats (r(2) = 0.49). Agreement was fair between LVEF values measured by the 2 methods (r(2) = 0.56). Normal rats had an average LVEF of 83.2% +/- 8.0% using PET and 81.6% +/- 6.0% using echocardiography. In rats with heart failure, LVEF was 54.6% +/- 15.9% using PET and 54.2% +/- 13.3% using echocardiography. CONCLUSION: Both PET and echocardiography clearly differentiated normal rats from rats with heart failure. Echocardiography is fast and convenient, whereas list-mode PET is also able to assess defect size, myocardial viability, and metabolism.
Angiotensin-converting enzyme inhibitors improve endothelial function, inhibit experimental atherogenesis, and decrease ischemic events. The Quinapril Ischemic Event Trial was designed to test the hypothesis that quinapril 20 mg/day would reduce ischemic events (the occurrence of cardiac death, resuscitated cardiac arrest, nonfatal myocardial infarction, coronary artery bypass grafting, coronary angioplasty, or hospitalization for angina pectoris) and the angiographic progression of coronary artery disease in patients without systolic left ventricular dysfunction. A total of 1,750 patients were randomized to quinapril 20 mg/day or placebo and followed a mean of 27 +/- 0.3 months. The 38% incidence of ischemic events was similar for both groups (RR 1.04; 95% confidence interval 0.89 to 1.22; p = 0.6). There was also no significant difference in the incidence of patients having angiographic progression of coronary disease (p = 0.71). The rate of development of new coronary lesions was also similar in both groups (p = 0.35). However, there was a difference in the incidence of angioplasty for new (previously unintervened) vessels (p = 0.018). Quinapril was well tolerated in patients after angioplasty with normal left ventricular function. Quinapril 20 mg did not significantly affect the overall frequency of clinical outcomes or the progression of coronary atherosclerosis. However, the absence of the demonstrable effect of quinapril may be due to several limitations in study design.