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PubMed1996

Medium-term effects of beta-blockade on left ventricular mechanics: a double-blind, placebo-controlled comparison of nebivolol and atenolol in patients with ischemic left ventricular dysfunction.

The aim of this study was to compare the effects on left ventricular function and exercise tolerance of a selective beta-antagonist (atenolol) with those of another selective beta 1-antagonist with vasodilator properties (nebivolol) in patients with ischemic left ventricular dysfunction but no overt congestive heart failure. Beta blockers are widely used in ischemic heart disease, but their effects on left ventricular mechanics and exercise tolerance are poorly defined in the subgroup of patients with significant systolic dysfunction but without clinical evidence of ischemia or congestive heart failure. Angiographic and symptom-limited exercise data were obtained at baseline and after an 8-10-week double-blind treatment with placebo (n = 10), 50 mg atenolol daily (n = 10), or 2.5 mg (n = 10) or 5 mg (n = 10) nebivolol daily. When compared to placebo, both atenolol and nebivolol reduced resting heart rate and improved left ventricular ejection fraction (from 33.9 to 39.2% with atenolol and from 36.5 to 40.8% with nebivolol, both P < .05) while lowering mean systolic wall stress. Only nebivolol, however, produced a parallel downward shift of the pressure-volume relationship during early diastolic filling and improved the early peak filling rate when compared to placebo (+ 10%, P < .05). When compared to baseline, maximal exercise duration increased by 7 and 13 seconds with placebo and atenolol, respectively (both NS vs baseline), and increased by 44 seconds with nebivolol (P = .0077 vs baseline). Both atenolol and nebivolol decreased maximal exercise heart rate; the reduction was more pronounced with atenolol. Prolonged beta 1-adrenoceptor blockade leads to a significant increase in left ventricular ejection fraction in patients with ischemic left ventricular dysfunction. The dissociation between the changes in resting left ventricular function and the changes in exercise duration suggests that in this clinical setting, the changes in systolic function may have less impact on functional capacity than an improvement in diastolic distensibility during the rapid filling phase.

Adrenergic beta-Antagonists↗

PubMed1985

Acute hemodynamic effects of propranolol, glycerylnitrate, and exercise in coronary patients with left ventricular dysfunction.

Some adverse effects of beta-blockers in heart failure are counteracted by glycerylnitrate. However, the hemodynamics in this condition after giving both drugs are not well known. We examined the drug combination in exercising coronary patients with left ventricular dysfunction. Elevated left ventricular end-diastolic pressure was a measure of dysfunction. A right-heart catheterization with three successive exercise stress tests was done in 40 patients. At repeated exercise without drugs a "warming up" phenomenon was observed, consisting of small but statistically significant reductions in pulmonary capillary wedge pressure, and heart rate. At exercise propranolol reduced heart rate, cardiac output, systemic blood pressure, left ventricular work, and increased arteriovenous oxygen difference. Glycerylnitrate reduced pulmonary capillary wedge pressure at exercise, but, contrary to the findings at rest, it did not increase heart rate or reduce cardiac output. The drug combination resulted in hemodynamics that were similar to those after propranolol alone, except for a lower pulmonary capillary wedge pressure. The drug combination allowed the patients to exercise with the benefits of the beta-blocker, but at a lower ventricular filling pressure. Thus, the potential hazard of giving beta-blockers to patients with left ventricular dysfunction may be reduced by adding glycerylnitrate.

Angina Pectoris↗

PubMed1992

Reversible and irreversible left ventricular dysfunction after acute myocardial infarction.

Left ventricular function after acute myocardial infarction depends on several mechanisms leading to left ventricular remodeling: (a) infarct size and healing and (b) adaptive changes involving both the dysfunctioning but viable myocardium (hibernating and stunned myocardium) and the nonischemic myocardium. The prognosis after acute myocardial infarction is strongly related to regional and global left ventricular function and the loss of dysfunctioning viable myocardium is a main factor in the worsening in left ventricular function in survivors of the acute phase. Thus, medical strategies should exert their beneficial effect on the "mechanical instability" of ventricular myocardium by saving the viable myocardium. beta-Blocker therapy has been shown to be effective in improving the prognosis via anti-ischemic and antiarrhythmic actions. The combination of metoprolol and nisoldipine seems to be able to preserve the contractile function of viable myocardium in the first 6 months after acute myocardial infarction.

Adrenergic beta-Antagonists↗

PubMed2000

Echocardiographic evaluation of left ventricular function in pure mitral stenosis.

Echocardiographic evaluation of left ventricular function was performed in 22 cases of pure rheumatic mitral stenosis and 22 age matched normal persons. Cases with any evidence of rheumatic activity in the preceding six months, those with gross tricuspid regurgitation and paradoxical movement of the interventricular septum and cases with atrial fibrillation were excluded. None of the patients showed systolic left ventricular dysfunction. Left ventricular end diastolic dimension was also not affected. Echocardiographic parameters did not have any relation for mitral valve area. Our observations show that mitral stenosis per se does not affect left ventricular function.

Adolescent↗

PubMed2004

Thiazolidinediones and congestive heart failure--exacerbation or new onset of left ventricular dysfunction?

BACKGROUND: Patients with diabetes mellitus have a high incidence of coronary heart disease and congestive heart failure (CHF). Thiazolidinediones (TZD) are a new class of pharmacological agents for the treatment of Type 2 diabetes mellitus, which have many beneficial cardiovascular effects. Peripheral oedema and weight gain have been reported in 4.8% of subjects on TZDs alone, with a higher incidence noted in those receiving combination insulin therapy (up to 15%), but there is limited data on the occurrence of CHF. METHODS AND RESULTS: In this paper, we report on six cases of TZD-induced fluid retention with symptoms and signs of peripheral oedema and/or CHF that occurred in subjects attending our diabetic clinic. The predominant finding in all cases was of diastolic dysfunction. All subjects were obese and hypertensive, with 5/6 having the additional risk factor of LVH, 5/6 subjects had microvascular complications, whilst 3/6 were also on insulin therapy. CONCLUSION: We suggest that obese, hypertensive diabetics may benefit from echocardiographic screening prior to commencement of TZDs, as these agents may exacerbate underlying undiagnosed left ventricular diastolic dysfunction.

Aged↗

PubMed1999

Independent prognostic information provided by sphygmomanometrically determined pulse pressure and mean arterial pressure in patients with left ventricular dysfunction.

OBJECTIVES: The purpose of this study was to evaluate the relationship of baseline pulse pressure and mean arterial pressure to mortality in patients with left ventricular dysfunction. BACKGROUND: Increased conduit vessel stiffness increases pulse pressure and pulsatile load, potentially contributing to adverse outcomes in patients with left ventricular dysfunction. METHODS: Pulse and mean arterial pressure were analyzed for their effect on mortality, adjusting for other modifiers of risk, using Cox proportional hazards regression analysis of data collected from 6,781 patients randomized into the Studies of Left Ventricular Dysfunction trials. RESULTS: Pulse and mean arterial pressure were related positively to each other, age, ejection fraction and prevalence of diabetes and hypertension and inversely to prior myocardial infarction and beta-adrenergic blocking agent use. Higher pulse pressure was associated with increased prevalence of female gender, greater calcium channel blocking agent, digoxin and diuretic use, lower heart rate and a higher rate of reported smoking history. Higher mean arterial pressure was associated with higher heart rate, lower calcium channel blocker and digoxin use and lower New York Heart Association functional class. Over a 61-month follow-up 1,582 deaths (1,397 cardiovascular) occurred. In a multivariate analysis adjusting for the above covariates and treatment assignment, higher pulse pressure remained an independent predictor of total and cardiovascular mortality (total mortality relative risk, 1.05 per 10 mm Hg increment; 95% confidence interval, 1.01 to 1.10; p = 0.02). Mean arterial pressure was inversely related to total and cardiovascular mortality (total mortality relative risk, 0.89; 95% confidence interval, 0.85 to 0.94; p <0.0001). CONCLUSIONS: One noninvasive blood pressure measurement provides two independent prognostic factors for survival. Increased conduit vessel stiffness, as assessed by pulse pressure, may contribute to increased mortality in patients with left ventricular dysfunction, independent of mean arterial pressure.

Adult↗

PubMed2005

Isovolumic but not ejection phase Doppler tissue indices detect left ventricular dysfunction caused by coronary stenosis.

BACKGROUND: Isovolumic acceleration (IVA) obtained by tissue Doppler echocardiography (TDE) is a sensitive and relatively load-independent index for assessing systolic ventricular function. IVA also has the ability to describe the force-frequency relationship during incremental atrial pacing in vivo. OBJECTIVE: We sought to assess the ability of IVA to detect global left ventricular (LV) dysfunction induced by coronary constriction. METHODS: In 6 open-chest anesthetized pigs we examined right ventricular and LV long-axis function by TDE (4-chamber view) with simultaneous invasive measurements of intraventricular pressure, maximum dP/dt, minimum dP/dt, and tau by microtip catheter. A pneumatic cuff was placed around the proximal portion of left anterior descending coronary artery (LAD) and distal flow was monitored by transonic flow probe. Mean arterial pressures were monitored by indwelling cannula. Baseline studies assessed force-frequency relationships with TDE and invasive measurements during incremental pacing from 100 to 200/min (20/min increments every 10 minutes). The protocol was repeated 10 minutes after balloon inflation to reduce LAD blood flow by 50%. RESULTS: Compared with baseline, LV pressure decreased significantly (P = .03, 2-way analysis of variance) as did maximum dP/dt (P < .004) with LAD constriction. At the same time IVA and isovolumic velocity at the LV free wall were significantly reduced (P < .002 and P = .04, respectively) and both IVA and isovolumic velocity were correlated with dP/dt (r = 0.45, P < .002, and r = 0.35, P < .02, respectively). TDE systolic indices were unchanged in the right ventricle. CONCLUSION: IVA detects changes in global LV systolic function during LAD constriction and may be a useful clinical tool to diagnose ischemia.

Animals↗

PubMed2006

Effects of altitude on effort tolerance in non-acclimatized patients with ischemic left ventricular dysfunction.

BACKGROUND: Few studies exist on the effects, in terms of work capacity and safety, of exposure to moderately high altitudes in patients with stable ischemic left ventricular dysfunction. Moreover no data are currently available on the cardiorespiratory response to walks in the mountains. AIM: The objective of this study is to evaluate the effects of altitude on effort tolerance during walks in the mountains and to determine whether exposure to altitude may be harmful to patients with ischemic left ventricular dysfunction. METHODS: Forty-five patients with stable chronic ischemic left ventricular dysfunction (ejection fraction=35+/-4%, and peak VO2>/=18/ml/kg per min in a preliminary effort test) were compared to 24 normal subjects. All subjects underwent a series of 6-min walking tests at three different altitudes: 500, 2000 and 2970 m above sea level. Cardiorespiratory response was assessed by a validated portable instrument. The resting arterial PO2 was measured at the three altitudes. RESULTS: No complications were observed during any tests in either the patients or the healthy controls. Overall, healthy subjects had higher values of 6-min walking test VO2 and walked longer distances in the test than did the patients with left ventricular dysfunction. The mean distances walked in the 6-min walking test were similar at 500 and at 2000 m in both the healthy controls and the patients; at 2970 m, however, the distances decreased in both groups, and more so in the patients (-11+/-3%) than in the controls (-5+/-2%) (P<0.01). VO2 during the 6-min walking test remained stable when the test was carried out at 500 and 2000 m (20.4+/-3.6 versus 19.9+/-4.1 ml/kg per min in patients, and 30.2+/-3.4 versus 29.8+/-4.2 ml/kg per min in the controls; P, NS), but decreased at 2970 m by 13.9+/-3% in patients (P<0.01) and by 6.6+/-2.1% in controls (P<0.01) (patients versus controls, P<0.01). Finally, a similar, significant decrease in arterial PO2 was observed in both groups only at 2970 m (-29%, P<0.01). CONCLUSION: Patients with stable ischemic left ventricular dysfunction had good tolerance while walking at high altitudes, but showed a moderate decrease in work capacity at 2970 m, which was greater than in normal subjects.

Acclimatization↗

PubMed2004

[Tachycardia-induced cardiomyopathy in children: a difficult diagnosis but a reversible form of left ventricular dysfunction].

UNLABELLED: Tachycardia-induced cardiomyopathy is a reversible left ventricular dysfunction caused by cardiac arrhythmia. Because of its reversibility, a correct diagnosis and treatment are necessary. The aim of our study was to precise the diagnostic procedures of the tachycardia-induced cardiomyopathy and to study the left ventricular function after the correction of the arrhythmia. PATIENTS AND METHODS: A retrospective study done between 1992 and 2001. Children studied were followed-up for: an idiopathic form of cardiomyopathy, in which the etiological research showed a cardiac arrhythmia; a cardiac arrhythmia associated to a cardiomyopathy. An electrocardiogram recorded the cardiac arrhythmia. The left ventricular function was evaluated by an echocardiography before and every month after the correction of the cardiac arrhythmia. RESULTS: Twelve children were included, ages ranged from 2 months to 15 years (median 11 years). Four patients presented a cardiac insufficiency associated to arrhythmia; three followed-up for an arrhythmia developed a cardiomyopathy; five whose cardiac arrhythmia was not easy to demonstrate had an idiopathic form of cardiomyopathy. The Wilcoxon test showed a significant amelioration (P < 0.01) of the left ventricular function after the correction of the cardiac arrhythmia. CONCLUSIONS: Tachycardia-induced cardiomyopathy in children is curable and the diagnosis is quite difficult. Pediatricians and family doctors should try to look for specific signs of cardiac insufficiency or arrhythmia. Pediatric cardiologists should search a tachycardia-induced cardiomyopathy in every idiopathic form of cardiomyopathy.

Adolescent↗

PubMed2001

Early autonomic and repolarization abnormalities contribute to lethal arrhythmias in chronic ischemic heart failure: characteristics of a novel heart failure model in dogs with postmyocardial infarction left ventricular dysfunction.

OBJECTIVES: Using a model of arrhythmias associated with ischemic left ventricular (LV) dysfunction, this study investigated autonomic and electrophysiologic mechanisms associated with sudden cardiac death (SCD) in chronic heart failure (HF). BACKGROUND: Left ventricular dysfunction from ischemic heart disease is associated with many instances of SCD. Electrophysiologic and autonomic derangements occur in HF, but their contribution to SCD risk is poorly understood. METHODS: Sudden death risk was assessed in 15 dogs with a healed anterior myocardial infarction (MI) during submaximal exercise and brief acute circumflex ischemia. Left ventricular dysfunction was then induced by repetitive circumflex microembolization until LV ejection fraction reached 35%. Before embolization, six dogs were susceptible to SCD, and nine were resistant. RESULTS: Baroreflex sensitivity was lower in susceptible dogs (10 ms/mm Hg +/- 4 ms/mm Hg vs. 20 ms/mm Hg +/- 11 ms/mm Hg, p = 0.04). QT intervals from susceptible dogs were longer after MI (246 ms +/- 26 ms susceptible vs. 231 ms +/- 20 ms resistant, p < 0.001) and prolonged within eight weeks after LV dysfunction was established (from 246 ms +/- 26 ms to 274 ms +/- 56 ms, +11%, p < 0.01). Heart rate in susceptible dogs increased during transient ischemia (+20%) and with progressive LV dysfunction (102 beats/min +/- 28 beats/min baseline to 154 beats/min +/- 7 beats/min LV dysfunction, p = 0.003). All susceptible dogs had spontaneous sustained ventricular tachycardia culminating in SCD. In contrast, QT intervals in resistant dogs prolonged after 24 +/- 6 weeks (from 231 ms +/- 20 ms to 238 ms +/- 15 ms, p < 0.05), and heart rates were unchanged. Only one resistant dog died suddenly with LV dysfunction. CONCLUSIONS: Depressed vagal and elevated sympathetic control of heart rate coupled with abnormal repolarization are associated with high SCD risk when post-MI LV dysfunction develops.

Animals↗

PubMed1984

The value of rest and exercise radionuclide ventriculography as compared to echocardiography and angiography in the detection of left ventricular dysfunction in patients with chronic aortic regurgitation.

Symptomatic patients with chronic aortic regurgitation and a left ventricular ejection fraction greater than 0.50, or forward cardiac index greater than 2.5 l/min/m2 at rest, have a much better survival rate than those with a depressed ejection fraction or cardiac index following aortic valve replacement. The annual mortality rate is approximately 2% for those with well preserved ventricular function versus 10% for those with depressed ventricular function at rest. This is in striking contrast to the situation that exists in patients with aortic stenosis, where the long-term survival is similar for those with a normal or depressed left ventricular ejection fraction or cardiac index at rest. Therefore, it would seem to be important to detect incipient left ventricular failure in patients with chronic aortic regurgitation and to intervene surgically before the left ventricular dysfunction becomes irreversible. In patients with a normal left ventricular ejection fraction at rest, maximal supine bicycle exercise testing with radionuclide ventriculography defines a group of patients with truly normal ventricular function (ejection fraction increases by greater than 0.05 ejection fraction units at peak exercise), and a group with incipient left ventricular dysfunction earlier than previously described variables (i.e., left ventricular ejection fraction at rest less than 0.50, left ventricular end-systolic volume index greater than 90 ml/m2, left ventricular end-systolic dimension greater than or equal to 5.5 cm, left ventricular shortening fraction less than or equal to 25%), and generally before the onset of symptoms.

Adolescent↗

PubMed2004

Selective microembolization of the circumflex coronary artery in an ovine model: Dilated, ischemic cardiomyopathy and left ventricular dysfunction.

BACKGROUND: Ventricular remodeling often occurs after myocardial infarction, yet the natural history remains unpredictable because of the chronicity of the process and therapeutic interventions involved. We induced cardiac dysfunction in an ovine model via selective microembolization of the circumflex coronary artery (LCx) to test the hypothesis that ventricular remodeling progresses following coronary microembolization for up to 24 months. Methods and results Sheep underwent weekly selective microembolization of the LCx until left ventricular ejection fraction stabilized <35% for 2 consecutive weeks. In a subgroup carried out to 4 months, the end-systolic pressure-volume relationship slope decreased from 2.3+/-0.6 (baseline) to 1.3+/-0.5 at month 4 (P<.05). In a second group, echocardiography at 24 months, the ejection fraction decreased from 51+/-3% (baseline) to 25+/-2% (month 5) (P<.05) and stabilized through month 24 (23+/-5%, P<.05), whereas left ventricular end-systolic area and left ventricular end-diastolic area increased by 222% and 98%, respectively, through month 24. CONCLUSIONS: Selective microembolization of the LCx induces left ventricular dysfunction followed by dilated, ischemic cardiomyopathy, which continues to progress for up to 2 years despite stabilization of left ventricular ejection fraction. This model of ventricular remodeling secondary to microinfarction may be a useful experimental platform for large animal heart failure investigations.

Animals↗

PubMed1997

Left ventricular dysfunction: a clue to cognitive impairment in older patients with heart failure.

OBJECTIVES: Cognitive impairment has been reported in middle aged patients with end stage heart failure. This cross sectional study assessed the prevalence and determinants of cognitive dysfunction in older patients with mild to moderate heart failure. METHODS: 57 consecutive patients (mean age 76.7 years) with chronic heart failure underwent physical examination, blood chemistry, urinalysis, chest radiography ECG, Doppler echocardiography, and the mini mental state examination (MMSE), mental deterioration battery, depression scale of the Center for Epidemiological Studies (CES-D), Katz activities of daily living, and instrumental activities of daily living 24 hours before hospital discharge. RESULTS: MMSE scores <24 were found in 53% of participants. The MMSE score was associated with left ventricular ejection fraction according to a non-linear correlation, so that cognitive performance was significantly lower in subjects with left ventricular ejection fraction < or =30%. The same pattern of correlation was evidenced between left ventricular ejection fraction and both the attention sub-item of MMSE and the Raven test score. In a multivariate linear regression model, after adjusting for age, sex, and a series of clinical data and objective tests, both age (beta=-0.30; P=0.038) and the natural log of left ventricular ejection fraction (beta=0.58; P=0.001) were associated with the MMSE score. CONCLUSION: Cognitive impairment in older patients with chronic heart failure is common, and independently associated with lower left ventricular ejection fraction. Given the overwhelming incidence and prevalence of heart failure in older populations, early detection of cognitive impairment in these subjects with prompt, intensive treatment of left ventricular systolic dysfunction may prevent or delay a remarkable proportion of dementia in advanced age.

Aged↗

PubMed1997

[Effect of diltiazem on cold-induced left ventricular dysfunction in patients with systemic sclerosis].

Patients with systemic sclerosis (SS) have cardiac dysfunction induced by cold exposure. We and others have demonstrated this finding after corporal chilling, suggesting a "coronary Raynaud phenomenon" mediated by intermittent vascular spasm. In this study we evaluated the effect of diltiazem (DTZ) in cardiac dysfunction induced by cold test in patients with SS without clinical evidence of heart disease. Twelve patients with SS were studied. One patient was excluded because he did not fulfill the prescribed treatment. Eleven patients (age of 49.9 +/- 3.8 years and illness duration of 9.3 +/- 4.8 years) were included. Gated equilibrium radionuclide ventriculography was recorded after red blood cells were labeled in vivo using an intravenous injection of stannous pirophosphate followed by 20 mc of 99 Tc (gamma camera with electrocardiographic R wave gating was used). Left ventricular injection fraction (LVEF) was calculated using computer analysis and wall motion abnormalities by visual interpretation. Patients were cooled using a thermic blanket set at 5 degrees centigrade. They were evaluated before and after a period of cooling. After corporal chilling LVEF decreased more than 10% in all of them. DTZ 270 mg a day was administered to the same patients during 48 hs. Basal and cold LVEF were repeated in all patients. The results with and without DTZ were compared by Student's t Test. The basal LVEF with and without DTZ was not different (64.8 +/- 2.6 and 63.1 +/- 1.8). After corporal chilling LVEF decreased (64.8 +/- 2.6 to 54.8 +/- 2.5 p < 0.00001) and reversible abnormalities in wall motion were noticed in patients without DTZ. When they received DTZ neither difference in LVEF (63.1 +/- 1.8 to 62.1 +/- 2.4) nor wall motion abnormalities were observed. We compared the LVEF after chilling (62.1 +/- 2.4 and 54.8 +/- 2.5) and we found an important difference with the use of DTZ (p < 0.005). It can be concluded that in patients with SS and no overt heart disease, DTZ prevents the early cardiac dysfunction induced by cold test. Probably this drug blunts the coronary spasm induced by cold test in this group of patients.

Body Temperature↗

PubMed2006

Inhibition of p38 mitogen-activated protein kinase attenuates left ventricular dysfunction by mediating pro-inflammatory cardiac cytokine levels in a mouse model of diabetes mellitus.

AIMS/HYPOTHESIS: We investigated the effect of SB 203580, a pharmacological inhibitor of p38 mitogen-activated protein kinase (MAPK), on cardiac inflammation, cardiac fibrosis, and left ventricular function using an animal model of diabetic cardiomyopathy. MATERIALS AND METHODS: Diabetes mellitus was induced by streptozotocin (50 mg/kg i.p. for 5 days) in 20 C57/BL6J mice. Diabetic mice were treated daily with the p38 MAPK inhibitor SB 203580 (1 mg/kg daily, n=10) or with placebo (n=10) and were compared to non-diabetic controls. Left ventricular function was measured by pressure-volume loops after 8 weeks of diabetes mellitus. The parameters for systolic function were the end systolic pressure-volume relationship (ESPVR) and the left ventricular end systolic pressure. The parameters for diastolic function were the left ventricular end diastolic pressure and the end diastolic pressure-volume relationship (EDPVR). Cardiac tissue was analysed by ELISA for the protein content of the cytokines TNF-alpha, IL6, IL1-beta, and TGF-beta1. Phosphorylation of MAPK p38 was analysed by western blot, and the total cardiac collagen content was analysed by Sirius red staining. RESULTS: Left ventricular dysfunction was documented by impaired ESPVR and EDPVR. Cardiac cytokine levels and cardiac fibrosis were increased in diabetic animals compared to controls. Treatment with the p38 inhibitor normalised cardiac cytokine levels and improved systolic function, but did not change cardiac fibrosis and diastolic dysfunction compared to placebo. CONCLUSIONS/INTERPRETATION: Pharmacological inhibition of p38 MAPK prevents cardiac inflammation and attenuates left ventricular dysfunction in diabetic cardiomyopathy.

Animals↗

PubMed1994

Norepinephrine-induced left ventricular dysfunction in anesthetized and conscious, sedated dogs.

These studies were conducted to evaluate effects of high dose norepinephrine infusion on left ventricular function in anesthetized and conscious dogs. Separate groups of pentobarbital anesthetized closed-chest dogs received norepinephrine infusion for 90 min followed by 1 h of recovery. Arterial pressure, electrocardiogram, two-dimensional echocardiogram and an equilibrium radionuclide angiogram were monitored. One hour following infusion of norepinephrine, left ventricular ejection fraction was reduced in a dose-dependent fashion. Fractional shortening was similarly reduced, with increased left ventricular systolic and diastolic dimensions also observed. Left ventricular end-systolic wall stress was increased at 60 min following infusion of norepinephrine but not saline: saline, 68 +/- 8, norepinephrine, 4 micrograms/kg/min, 113 +/- 8 g/cm2. The left ventricular end-systolic wall stress/fractional shortening relationship showed reduction of contractility. In 10 conscious dogs pretreated with morphine, norepinephrine at 5 micrograms/kg/min x 90 min produced similar changes to those seen in anesthetized animals. Ejection fraction was reduced from 0.69 +/- 0.3 to 0.36 +/- 0.04 at 60 min post infusion. Fractional shortening was also reduced. Left ventricular end-diastolic dimension was increased. However, when animals were followed for 1 week, complete recovery occurred within 48 h. Histology showed mild contraction band necrosis in acute experiments and mild perivascular fibrosis in chronic experiments. Therefore, norepinephrine cardiotoxicity produced significant left ventricular dilation and reduction of ejection phase indices of left ventricular function associated with reduced contractility. In chronic dogs, histologic changes were mild, and left ventricular dysfunction was reversible.

Anesthesia↗

PubMed1980

Aortocoronary bypass in patients with severe left ventricular dysfunction.

The results of aortocoronary bypass grafting in 29 patients with severe left ventricular dysfunction (ejection fraction less than 35%) were studied. All patients had severe angina pectoris; 17 patients has class IV heart function and 12 had class III function according to the New York Heart Association classification. Intra-aortic balloon pump support was instituted preoperatively in all patients. Three patients died in the perioperative period. Survivors were followed up for a mean period of 20 months; there were three late deaths. Sixteen patients were clinically improved; 8 had class I and 8 class II heart function at follow-up. Fourteen patients underwent cardiac catheterization postoperatively at a mean time of 19 months. Although 22 (79%) of the 28 grafts were patent, there was no significant improvement in resting left ventricular dysfunction as assessed by ejection fraction, left ventricular volume or left ventricular end-diastolic pressure. Furthermore, graft patency could not be correlated with improvement in segmental wall motion. There was a 10% operative and an 11.5% late mortality and no measurable improvement in resting left ventricular function in this study but the majority (73%) of the surviving patients experienced definite clinical improvement.

Angina Pectoris↗

PubMed1994

Survival after percutaneous transluminal coronary angioplasty in patients with severe left ventricular dysfunction.

To assess the effects of coronary angioplasty in patients with severe left ventricular dysfunction, the results of procedures, performed between 1987 and 1991, in 100 patients (90 male) with left ventricular function < or = 0.35 (range, 0.20 to 0.35) and anginal symptoms were analyzed. Mean age was 62 +/- 10 years (range, 38 to 85 years). Ninety-five patients had previous myocardial infarction and 27 patients had previous coronary artery bypass grafting. Unstable angina was present in 81 percent of patients. Single-vessel disease was present in 6 patients, double vessel was present in 31 patients, and triple-vessel disease was present in 63 patients. Percutaneous transluminal coronary angioplasty (PTCA) was attempted on 164 vessels, 27 of these with chronic total occlusion. The overall angiographic success rate was 84 percent. Myocardial infarction occurred in four patients, six patients underwent urgent coronary bypass surgery, and seven patients died of cardiac causes. There was a 9 percent incidence of total in hospital mortality. Major complications were significantly more frequent in patients with triple-vessel disease. Clinical success was achieved in 75 patients, 55 of these with incomplete revascularization. Long-term follow-up (mean, 19 +/- 7 months) was available in all patients with clinical success. Thirteen patients had repeated PTCA, 8 patients had coronary surgery, and 13 patients died. In conclusion, in patients with severe left ventricular dysfunction, acute complications and late mortality rate are high. Patients with triple-vessel disease are a higher risk subset and have no long-term benefits by PTCA.

Angioplasty, Balloon, Coronary↗