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Effects of antiarrhythmic agents on left ventricular function during exercise in patients with chronic left ventricular dysfunction.

This study was designed to determine the effects of antiarrhythmic agents on global left ventricular (LV) function during exercise in patients with chronic LV dysfunction. Thirty-five patients with LV dysfunction [LV ejection fraction (LVEF) < 45%] and ventricular arrhythmias were studied. They were randomly classified into 3 groups: patients who received a single oral dose of 6 mg/kg disopyramide phosphate (n = 12), those who received a single oral dose of 4 mg/kg mexiletine hydrochloride (n = 12), and those who received a single oral dose of 4 mg/kg pilsicainide hydrochloride (n = 11). First, all patients were subjected to baseline rest and peak exercise, equilibrium-gated cardiac-pool scintigraphy with 99mTc-human serous albumin of 740 MBq (baseline data). Second, on a separate day, they were given drugs once, and were subsequently subjected to rest and peak exercise equilibrium-gated cardiac-pool scintigraphy. Exercise LVEF and peak ejection rate (PER) after administration were significantly lower in the disopyramide and pilsicainide groups than in the mexiletine group (p < 0.05, respectively). The changes in LVEF and PER from rest to peak exercise after administration were significantly less than the baseline changes in those in the disopyramide and pilsicainide groups (p < 0.05, respectively). However, no significant changes in functional parameters were recognized in the mexiletine group. Due care should be taken when disopyramide and pilsicainide are administered to patients with chronic LV dysfunction since they reduce systolic LV function during exercise.

Aged↗

Gender differences in systolic left ventricular function in hypertensive patients with electrocardiographic left ventricular hypertrophy (the LIFE study).

Echocardiography was performed in 944 untreated hypertensive patients (391 women and 553 men, mean age 66 years) who had electrocardiographic left ventricular (LV) hypertrophy at baseline in the Losartan Intervention For End point reduction in hypertension (LIFE) study to evaluate gender-associated differences in systolic LV function. Women had significantly lower diastolic blood pressure (175/97 vs 173/99 mm Hg) and body surface area and a higher body mass index (all p < 0.01). Women also had higher LV ejection fraction (EF), endocardial and midwall fractional shortening (63% vs 60%, 35% and 33%, and 16% vs 15%, respectively, all p < 0.01), higher stress-corrected midwall fractional shortening (98% vs 96%, p < 0.05), and lower circumferential end-systolic wall stress (178 vs 187 kdynes/cm(2), p < 0.01). There was no difference in age or LV mass indexed for height(2.7), but relative wall thickness was higher in women (0.42 vs 0.41, p < 0.05). In multiple regression analyses: (1) EF and endocardial fractional shortening were 2% to 3% higher in women than men, independent of the effects of LV stress, body mass index, and height (multiple r = 0.77 and 0.75, respectively, gender p < 0.02 in both models); (2) midwall fractional shortening was 0.5% higher in women, independent of the effects of age, body mass index, circumferential end-systolic stress, and absence of diabetes (multiple r = 0.36, p = 0.014 for gender); and (3) stress-corrected LV midwall fractional shortening was 2% higher (p = 0.004) in women, independent of the effects of age, height, heart rate, body mass index, and diabetes (multiple r = 0.33). Thus, female gender is an independent predictor of higher systolic LV function in hypertensive patients with electrocardiographic LV hypertrophy.

Aged↗

Left ventricular function during support with an asynchronous pulsatile left ventricular assist device.

BACKGROUND: Left ventricular assist devices (LVADs) are frequently used to maintain patients with severe heart failure until heart transplantation becomes possible. Some patients may experience recovery of LV function during such support. Therefore, it is essential to be able to monitor changes in LV function in this setting. METHODS: We studied LV function in 10 patients (median age 34 years, 9 male) who had LVADs implanted because of severe heart failure due to dilated cardiomyopathy a median of 4 months previously. Median pre-implant ejection fraction was 27% and all patients had been on maximal medical therapy, including intravenous inotropic support, prior to insertion of the LVAD. RESULTS: During LVAD support there were cyclical variations in LV dimensions, fractional shortening (FS) and transmitral flow, related to changes in the phase relationship of the LV and the LVAD. The "best" FS occurred when LV systole coincided with device filling and the "worst" FS when LV systole coincided with device ejection. Median FS with the pump switched off was 18% (10% to 32%). Pump-off FS was significantly greater than the "worst" FS with the pump on (5%, p = 0.002), and similar to the "best" pump-on FS (19%, p = NS). CONCLUSIONS: LV function could be studied echocardiographically during LV support and brief periods of interruption in support. Function varied according to the phase relationship of the LV and LVAD. The "best" FS measured during LVAD support was more closely related to the FS with the device switched off than the "worst" pump on FS. The "best" pump-on LV function is therefore most representative of intrinsic LV performance and can be used as a guide to recovery and the potential need for pump-off studies.

Adult↗

Right latissimus dorsi cardiomyoplasty improves left ventricular function by increasing peak systolic elastance (Emax).

BACKGROUND: Dynamic cardiomyoplasty remains a promising but poorly understood surgical modality for selected patients with dilated cardiomyopathy. Despite encouraging clinical results, objective evidence of enhanced ventricular function using traditional indexes (cardiac output, ejection fraction, and dP/dt) has been difficult to document after cardiomyoplasty. Several investigators have suggested that cardiomyoplasty acts partly by unloading the left ventricle. These indexes all depend somewhat on loading conditions, however, and might not detect such an interaction. The time-varying elastance model provides an index of contractility, Emax, that is relatively insensitive to changes in loading conditions. We applied this model to study the effect of right latissimus dorsi cardiomyoplasty on left ventricular function in an acute canine model. METHODS AND RESULTS: Five dogs underwent acute cardiomyoplasty using untrained right latissimus dorsi muscle. Instrumentation included Millar pressure transducers in the left ventricle and aortic root, an electromagnetic flow probe around the ascending aorta, and a volume conductance catheter in the left ventricle. A cuffed nerve electrode around the thoracodorsal nerve and a right ventricular sensing lead were connected to a Medtronic Cardiomyostimulator (5 V, 30 Hz, 1:1 synchronization). Transient caval occlusions were performed with the stimulator both off and on to calculate Emax and the slope of the end-systolic pressure-volume relationship (Ees). Turning the stimulator on significantly increased peak systolic elastance (Emax) and end-systolic elastance (Ees) in all five dogs by an average of 56% and 78%, respectively (P < .05). End-diastolic volume and end-systolic volume decreased by 18% and 28%, respectively (P < .05). All other measured hemodynamic parameters, including peak left ventricular pressure, mean arterial pressure, cardiac output, stroke volume, stroke work, ejection fraction, preload-recruitable stroke work, and dP/dt, did not change significantly. CONCLUSIONS: These results show that, in this acute canine model, right latissimus dorsi cardiomyoplasty significantly improves left ventricular function while decreasing left ventricular volumes. The results are consistent with the theory that cardiomyoplasty increases contractility while unloading the ventricle by decreasing end-diastolic volume. This increase in Emax despite inconsistent changes in other indexes underlies the importance of using load-insensitive indexes of ventricular function when studying cardiomyoplasty.

Animals↗

Left ventricular function in acute myocardial infarction.

Left ventricular catheterization was carried out in 40 patients with acute myocardial infarction. Left ventricular end-diastolic pressure (LVEDP) was elevated in 85% of the patients studied. In 14 patients with apparently uncomplicated infarcts, LVEDP averaged 15 mm Hg, and cardiac index (2.98 liter/min/m(2)), stroke volume (38.3 ml/m(2)), and stroke work (49.2 g-m/m(2)) were within normal limits. In 12 patients with clinical signs of left ventricular failure, LVEDP averaged 29.9 mm Hg, cardiac index was at the lower limit of normal (2.79 liter/min/m(2)), but stroke volume (31.6 ml/m(2)) and stroke work (37.3 g-m/m(2)) were reduced. In 14 patients with clinical signs of shock, LVEDP averaged significantly lower than in the heart failure group (21.1 mm Hg), but cardiac index (1.59 liter/min/m(2)), stroke volume (16.5 ml/m(2)), and stroke work (11.1 g-m/m(2)) were markedly reduced. A large presystolic atrial "kick" (average amplitude 9.5 mm Hg) was an important factor in the high LVEDP in the patients with heart failure but not in those with shock. The first derivative of left ventricular pressure was significantly lower in shock than in the nonshock group. Although right atrial pressure (RAP) and LVEDP were significantly correlated (r = 0.49), wide discrepancies in individual patients rendered the RAP an unreliable indicator of the magnitude of left ventricular filling pressure. THESE DATA SHOW THE FOLLOWING: (a) LVEDP is usually elevated in acute myocardial infarction, even in absence of clinical heart failure; (b) cardiac output apparently is supported by increased LVEDP and compensatory tachycardia; (c) in patients with shock, left ventricular function usually is markedly impaired, but inadequate compensatory cardiac dilatation or tachycardia could contribute to the reduced cardiac output in some individuals; (d) lower LVEDP in shock than in heart failure may represent differences in left ventricular compliance.

Adult↗

Triiodothyronine-enhanced left ventricular function after ischemic injury.

Hypothyroidism is associated with profound left ventricular dysfunction. Brain-dead organ donors and patients undergoing cardiopulmonary bypass are chemically hypothyroid with significantly reduced circulating free triiodothyronine (T3). To test the hypothesis that T3 enhances left ventricular function in a hormonally deficient environment, a total of 36 healthy New Zealand White rabbit hearts were studied using a modified Langendorff preparation with Krebs-Henseleit perfusate and intra-ventricular balloon. In 9 normal rabbit hearts a cumulative dose-response curve with logarithmically increasing doses of T3 was obtained. The vehicle solution for T3 dissolution served as control (n = 9). Left ventricular function was assessed from peak developed pressure at baseline and after T3 administration. Triiodothyronine had no effect in normal hearts on peak developed pressure or end-diastolic pressure. In 18 rabbits, the acute effect of T3 administration after ischemia was investigated. Preischemic left ventricular function was measured to serve as baseline, and hearts were subjected to 37 degrees C global ischemia. Triiodothyronine (n = 9) or vehicle (n = 9) was infused during reperfusion, and left ventricular peak developed pressure was measured at 30 and 60 minutes of reperfusion. Recovery of function (expressed as percent return of left ventricular peak developed pressure) was significantly improved within 15 minutes of reperfusion (65.0% +/- 2.1% versus 80.2% +/- 4.1%) and remained significantly improved throughout the reperfusion period (p less than 0.05 by analysis of variance). These data suggest that although T3 possesses no inotropic properties, it significantly improves postischemic left ventricular function. The rapidity of the functional improvement suggests that these effects may be due to plasma membrane-mediated mechanisms.

Animals↗

Tissue tracking allows rapid and accurate visual evaluation of left ventricular function.

AIMS: To evaluate the ability of tissue tracking for rapid assessment of left ventricular function by determination of the systolic mitral annular displacement. Tissue tracking is a new echocardiographic modality based on Doppler Tissue imaging allowing rapid visual assessment of the systolic baso-apical displacement of each myocardial segment in apical views by a graded colour display. METHODS AND RESULTS: We studied 90 patients (69 male, age 60.4 +/- 10.1 years) with different left ventricular function (25 subjects with normal left ventricular function, 25 patients with homogeneous depression of left ventricular function and 40 patients with prior myocardial infarction). Systolic mitral annular displacement was determined by tissue tracking and M-mode echocardiography. Apical two-, three- and four-chamber views were used to determine the mitral annular displacement of six sites. Left ventricular ejection fraction was determined by two-dimensional echocardiography using Simpson's rule. Tissue tracking was possible in all patients. In the 50 patients with normal left ventricular function or homogeneous depression of left ventricular function, mean mitral annular displacement correlated closely with mitral annular displacement determined by M-mode (r=0.99,P <0.001) and with left ventricular ejection fraction (r=0.97, P<0.001). Left ventricular ejection fraction < or = 30% could be predicted with a sensitivity of 98% and a specificity of 78% using a cut-off value of 4.8mm for the mitral annular displacement determined by tissue tracking. In patients with prior myocardial infarction correlation between the mean mitral annular displacement and left ventricular ejection fraction was lower (r=0.87, P<0.001). CONCLUSION: Systolic mitral annular displacement determined by tissue tracking correlates closely with mitral annular displacement determined by M-mode and with left ventricular ejection fraction. Thus, tissue tracking allows rapid semiquantitative evaluation of global left ventricular function by assessment of systolic mitral annular displacement.

Aged↗

Left ventricular function in acute myocardial infarction: assessment by nuclear angiography.

Left ventricular function was assessed in 38 patients two to six days after acute myocardial infarction using nuclear angiocardiography and the following parameters were measured: Left ventricular end-diastolic (LVEDV) and end-systolic volumes (LVESV), ejection fraction (LVEF), indices of left ventricular filling and emptying, right ventricular ejection fraction and ejection rate. Their clinical significance was assessed by their relationship to the patients site and size of infarction, functional capacity, morbidity and mortality. The most sensitive indices of depressed left ventricular function were the EF and ESV. Thus, function was preserved in patients with a small inferior infarction (LVEF = 0.57 +/- 0.07, LVESV = 69 +/- 14 ml) and in Killip Class I (LVEF = 0.48 +/- 0.13, LVESV = 80 +/- 20 ml). Function was disturbed most in patients with extensive anterior infarction (LVEF = 0.18 +/- 0.12, LVESV = 131 +/- 46 ml), Killip Class IV (LVEF = 0.13 +/- 0.07, LVESV = 160 +/- 35 ml), cardiogenic shock (LVEF = 0.14 +/- 0.07, LVESV = 160 +/- 35 ml), pulmonary edema (LVEF = 0.11 +/- 0.06, LVESV = 166 +/- 25 ml) and pulmonary capillary wedge pressure greater than 20 mm Hg (LVEF = 0.14 +/- 0.07, LVESV = 160 +/- 33 ml). Previous infarction was associated with LV dilatation and a greater LVEDV. A lower ejection fraction signified a large infarct and poor left ventricular function. If the ejection fraction was less than 0.15, the patients were unlikely to leave the hospital alive, or if less than 0.25, they were left with poor residual ventricular function and either had significant cardiac failure or high late mortality. Nuclear angiocardiography was a simple method of predicting the clinical pattern and prognosis in each patient and emphasized the importance of limiting infarct size in acute myocardial infarction.

Adult↗

Effects of insulin on left ventricular function during dynamic exercise in overweight and obese subjects.

AIMS: We designed this study in order to determine the effect of insulin on cardiac function in overweight and obese subjects during exercise. METHODS AND RESULTS: The cardiac function of 62 normal glucose tolerant subjects, aged 30-40 and divided into normal weight (group 1, n=22, BMI 20-24.9 kg/m(2)), overweight (group 2, n=20, BMI 25-29.9 kg/m(2)), and obesity (group 3, n=20, BMI 30-35 kg/m(2)) was evaluated at rest and during dynamic exercise through angiocardioscintigraphy, when on hyperinsulinaemic euglycaemic clamp (test A) and when on normal saline infusion (test B). Left ventricular function at rest was statistically greater (P<0.05) in both tests in overweight and obese subjects compared with normal weight controls, with no statistical difference (P=0.057) within groups between insulin and normal saline infusion. During exercise, cardiac function improved in all the subjects in both tests. The increase was lower in overweight and obese patients, even if statistically significant only in obese vs. control subjects in both tests (P<0.05). Insulin sensitivity showed a significant correlation (P< or =0.001) with left ventricular ejection fraction (LVEF) at rest and with change in LVEF during clamp. CONCLUSION: Our findings suggest a metabolic pathogenesis for the impaired LV function in obesity.

Adult↗

[Short term simvastatin use in patients with heart failure of ischemic origin. Changes of blood lipids, markers of inflammation and left ventricular function].

AIM: To study changes of left ventricular function and some markers of inflammation during use of simvastatin in patients with ischemic systolic heart failure. METHODS: Statin naive patients (n=70) with coronary heart disease (CHD), NYHA class II-IV HF and LV ejection fraction (EF) 35% or less after 1 month of stabilization were randomized to simvastatin 40 mg/day (n=36) or no statin (n=34). Lipids, tumor necrosis factor alpha (TNF), and C-reactive protein (CRP) were measured and echocardiography carried out at baseline and in 4 months. In patients with sinus rhythm (n=48) left ventricular diastolic function was assessed by Doppler echo. Seven patients were not restudied and analysis included data from 32 (statin) and 31 (control) patients. RESULTS: Groups were similar except baseline CRP which was significantly higher in controls. In statin treated patients reduction of low density lipoprotein (LDL) cholesterol (CH) was 42%, triglyceride levels also significantly decreased. High density lipoprotein CH rose by 14.4 and 12.9% in statin and control groups, respectively. Despite lower initial level decrease of CRP was significant only in statin group. No significant changes of TNF occurred in either group. Left ventricular EF rose equally in statin treated (+5.7+/-4.7%) and untreated (+4.1+/-4.6%) patients (p=ns). Significant increase of peak atrial filling velocity (A) and decrease of E/A in statin group were difficult to interpret in the presence of systolic dysfunction. CONCLUSION: Short term simvastatin use in patients with systolic heart failure due to CHD caused lowering of LDLCH and CRP however this was not associated with changes of left ventricular EF different from those in control group.

Aged↗

Noninvasive evaluation of left ventricular function in chronic severe anemia.

Left ventricular function was evaluated noninvasively in cases of chronic severe anemia (CSA) by recording systolic and diastolic time intervals (STI and DTI). These time intervals were recorded in 38 patients with CSA (hemoglobin below 7 g%), without cardiac decompensation, and in 30 control subjects. STI and DTI were measured from the simultaneous recordings of the apexcardiogram, carotid arterial pulse, electrocardiogram and phonocardiogram. The left ventricular ejection time was significantly prolonged (p less than 0.02), and associated with marked shortening of the PEP and reduction of the PEP/LVET ratio (p less than 0.001 in each case) in cases of CSA as compared to controls. Regarding the DTI, there was significant shortening of total filling time, slow filling time (p less than 0.001 in each case) and atrial systole (p less than 0.01) with no appreciable change in rapid filling time and isovolumic relaxation time. The SFT/RFT ratio and a/H ratio (the amplitude of the a-wave relative to the total height of the apexcardiogram) showed significant reductions (p less than 0.001 in each case). These changes in STI and DTI indicate enhanced left ventricular performance during diastole followed by faster and more complete relaxation during diastole in CSA.

Adult↗

Effect of hormone replacement therapy on lipids and left ventricular function in postmenopausal smokers.

OBJECTIVE: Menopause and smoking have negative effects on the cardiovascular system. The study was planned to investigate the influence of oral hormone replacement therapy (HRT) on heart function and lipids in postmenopausal smokers. METHODS: Lipid levels and left ventricular systolic and diastolic function by means of echocardiography were assessed before entering the study and at 6-month intervals during the 12 months of oral HRT in 62 postmenopausal women, 30 of whom were smokers and 32 were non-smokers. RESULTS: Oral HRT caused a significant decrease in levels of total cholesterol and low density lipoprotein (LDL) cholesterol and a significant increase in high density lipoprotein (HDL) cholesterol in non-smokers. This effect was not evident in smokers. Echocardiography revealed a significant improvement of systolic function (ejection fraction, left ventricular outflow tract velocity, forward velocity integral, acceleration time and mean systolic acceleration) and diastolic function (diastolic time, duration of the early filling phase, peak velocity of early mitral flow, and the ratio of late to early peak mitral flow) in non-smokers. In smokers, a significant increase in some parameters of systolic function (ejection fraction, acceleration time and mean systolic acceleration) and an insignificant change in diastolic function were observed. Oral HRT of 12 months' duration has very limited beneficial effects on CONCLUSION: lipids and left ventricular heart function in postmenopausal women who smoke.

Administration, Oral↗

[Left bundle-branch block: inferences from ventricular septal motion in the echocardiogram concerning left ventricular function].

In left bundle branch block (LBBB) abnormal motions of the interventricular septum (IVS) are well known in echocardiography. We asked: (1) Is it possible to distinguish several kinds of IVS motion in the M-mode echocardiogram and (2) Is there any correlation with clinical data? We analyzed the M-mode echocardiograms of 100 patients in whom LBBB had been diagnosed, either alone or in connection with latent or dilatative cardiomyopathy. All showed a posterior motion of the IVS in early systole. Three kinds of motion could subsequently be identified: anterior (= paradox) (18%, type A), posterior (= normal) (58%, type B), and intermediate (24%, type AB). Group A had a more severe clinical stage of disease than group B (p less than 0.0005); ECG showed a longer QRS complex (p less than 0.0005), X-ray a bigger cardiac-thoracic ratio (p less than 0.0005), and M-mode-echocardiogram larger left ventricular end-diastolic diameters (p less than 0.025). Mean values of group AB fell between those of group A and those of group B. Moreover, ejection fraction at left ventricular angiography was lower in group A (52.0%) than in groups AB (58.0%) and B (62.9%) (A vs B p less than 0.005), and mean pulmonary artery pressure on exertion was higher in group A (43.3 mm Hg) than in groups AB (38.1 mm Hg) and B (28.7 mm Hg) (A vs. B p less than 0.0005). For types A and AB taken together, the likelihood of abnormal pulmonary artery pressure on exertion was 88%.(ABSTRACT TRUNCATED AT 250 WORDS)

Bundle-Branch Block↗

Postoperative left ventricular function in patients with mitral stenosis. The effect of commissurotomy and valve replacement on left ventricular systolic function.

Preoperative and postoperative left ventricular cineangiograms of 26 patients with mitral stenosis (MS) were analyzed to calculate left ventricular end-diastolic volume (EDV), end-systolic volume (ESV), stroke volume (SV), ejection fraction (EF) and systolic regional wall motion. Nine patients underwent commissurotomy (OMC group) and 17 patients underwent mitral valve replacement (MVR group). In both groups, postoperative EDV, SV and EF tended to increase, while ESV remained unchanged. In the OMC group, systolic wall motion of the left ventricle was found to be improved postoperatively, whereas systolic wall motion in the MVR group was found to be impaired postoperatively. The latter finding was assumed to be due to excision of the papillary muscles and chordae tendineae. Preservation of these structures is likely to be important for better postoperative functional recovery of the left ventricle.

Adult↗

Fentanyl-droperidol-nitrous oxide anaesthesia in patients with ischaemic heart disease and various degrees of left ventricular functional impairment.

Haemodynamic stability and left ventricular function (LVF) during induction of anaesthesia and sternotomy were compared in three groups of patients with ischaemic heart disease, angiographically classified as having good, poor and depressed LVF. Anaesthesia was given with fentanyl-droperidol and nitrous oxide. The group with good LVF showed large variations in arterial pressure and heart rate between stimulated and unstimulated states with a reasonable preservation of LVF, expressed as stroke volume, through the whole observation period. The group with poor LVF showed monotonously falling arterial pressure, and no heart rate response to tracheal intubation. These patients maintained remarkably stable stroke volumes in connection with low afterloads. After nitrous oxide, additional volume loading was required because of profound hypotension. The majority of the patients in the intermediate group, labelled "depressed LVF", reacted to intubation and sternotomy with signs of left ventricular failure in connection with tachycardia and increased afterloads. The individual variations between patients with different degrees of left ventricular impairment were considerable, and these haemodynamic patterns need to be confirmed with a larger material.

Anesthesia, General↗

Systemic, pulmonary, and renal hemodynamic effects of endothelin ET(A/B)-receptor blockade in patients with maintained left ventricular function.

Endothelin-1 (ET-1) regulates vascular tone in congestive heart failure and modulates renal function. Its role in patients with normal left ventricular (LV) function and its renal effects are unclear. Cardiac and renal hemodynamics were studied in 24 patients with normal LV function and coronary arteries after single-dose, double-blind, randomized administration of TAK-044 (25, 50, or 100 mg, i.v.), an ET(A/B)-receptor antagonist, or placebo. Hemodynamics were monitored using Swan-Ganz and arterial catheters, and ET levels were measured. Renal function was assessed by clearance techniques. In the absence of a dose-response relation, TAK-044 patients were analyzed as a single group. Most hemodynamic effects occurred during the first 4 h. TAK-044 reduced mean arterial (-9.3 mm Hg, p < 0.001), pulmonary (-1.8 mm Hg, p = 0.01), and pulmonary capillary wedge pressure (-1.6 mm Hg, p < 0.001) between 30 min and 4 h. Mean reduction in systemic vascular resistance was 279 dyne/s/cm2 (p < 0.001), whereas heart rate increased 6.1 beats/min (p < 0.001) and cardiac index by 0.37 L/m2 (p = 0.01). Stroke volume index, right atrial pressure, and pulmonary vascular resistance did not change. TAK-044 increased renal plasma flow in proportion to the increase in cardiac output (+119 ml/min, 4 h after TAK-044; p < 0.05) and ET-1 levels (2.5-fold; p < 0.05). No serious side effects were noted. In patients with normal cardiac function, ET-receptor blockade causes vasodilation and reduces systemic but not pulmonary vascular resistance and increases cardiac index and renal plasma flow.

Aged↗

Left stellate ganglion block has only small effects on left ventricular function in awake dogs before and after induction of heart failure.

Left stellate ganglion block (LSGB) results in acute sympathetic denervation of the left ventricular (LV) posterobasal wall. We investigated the effects of LSGB in chronically instrumented awake dogs before and after the induction of pacing-induced congestive heart failure. Twelve dogs were instrumented for measurement of global hemodynamics [LV pressure (LVP)], its first derivative (dP/dt), cardiac output (CO), and regional myocardial function (systolic posterobasal segment length shortening, mean velocity [SLmv]). Before the induction of heart failure (n = 12), LSGB did not affect CO [3.2+/-1.4 (control, mean +/- SD) vs. 3.3+/-1.6 L/min (LSGB, P = 0.45)] and SLmv (11.1+/-4.0 vs. 10.8+/-4.0 mm/s, P = 0.16), but slightly reduced LVP (130+/-12 vs. 125+/-14 mm Hg, P = 0.04), dP/dt(max) (3614+/-755 vs. 3259+/-644 mm Hg/s, P = 0.003) and dP/dt(min) (-3153+/-663 vs. -2970+/-725 mm Hg/s, P = 0.03). During heart failure (n = 8), global hemodynamics [CO (2.8+/-1.2 vs. 2.7+/-1.2 L/min, P = 0.04), LVP (119+/-6 vs. 112+/-9 mm Hg, P = 0.01), dP/dt(max) (1945+/-520 vs. 1824+/-554 mm Hg/s, P = 0.03) and dP/dt(min) (-2402+/-678 vs. -2243+/-683 mm Hg/s, P = 0.04)], as well as regional myocardial function, were significantly different after LSGB [SLmv] (8.0+/-3.8 vs. 6.9+/-3.4 mm/s, P = 0.02)]. In conclusion, even during heart failure, the hemodynamic changes after LSGB are small, confirming its broad margin of safety.

Anesthetics, Local↗

Effects of transdermal nitroglycerin on left ventricular function after acute myocardial infarction.

Progressive left ventricular dysfunction in acute myocardial infarction patients is associated with a poor prognosis. It has been shown that some therapeutic measures which have the potential for limiting the infarct size and preserving ventricular function, are also able to reduce the incidence of congestive heart and improve survival. The aim of this protocol was to assess the effects of transdermal nitroglycerin administered within 72 hours after the onset of acute myocardial infarction and for the following 6 months, on left ventricular function. A total of 98 consecutive acute myocardial infarction patients were randomly allocated, within 72 hours of onset of symptoms, to a double-blind 6-month-therapy with either 10 mg/24 hour transdermal nitroglycerin or placebo. Patients underwent two-dimensional echocardiography at entry, after 2 weeks, 3 months and 6 months. In the nitroglycerin group, end-diastolic volume increased during the follow-up (+6.7%, p < 0.05) while end-systolic volume remained nearly unchanged; ejection fraction and stroke volume increased progressively (+6.3%, p < 0.05, +14.2%, p < 0.05, respectively) and a important reduction of percent of dyssynergic segments was present (-19.2%, p < 0.005). In the placebo group end-diastolic volume and end-systolic volume slightly increased during the follow-up (+2% and +4.9% respectively); ejection fraction and stroke volume remained nearly unchanged during the study; percent of dyssynergic segments showed an important decrease after 2 weeks and 6 months (-21.3%, p < 0.005). A clinically relevant increase (> 20%) in ejection fraction was present more frequently in the nitroglycerin than in the placebo group (p < 0.001). In conclusion, the early (within 72 hours) and prolonged (6 months) administration of transdermal nitroglycerin in acute myocardial infarction improves ejection fraction and stroke volume but does not modify ventricular remodeling.

Acute Disease↗