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PubMed1991

Clinical heart failure trials and the design rationale of Studies of Left Ventricular Dysfunction (SOLVD).

Heart failure has become a major worldwide public health problem. Several million patients suffer with this malady and large epidemiologic studies have documented mortality that can be in excess of 50% at 5 years. Furthermore, morbidity is great with this disease and hospitalizations are increasing yearly. Attention must be placed on pharmacotherapeutic strategies that can attenuate the morbidity and high mortality seen in the heart failure milieu. Studies of Left Ventricular Dysfunction (SOLVD) is a large, multicenter, multinational, clinical research program with two, double-blind, randomized clinical trials designed to evaluate the effects of an angiotensin converting enzyme inhibitor, enalapril, on heart failure morbidity and mortality. The program also includes a registry and several substudies that are designed to better clarify heart failure pathophysiology. With over 13,000 subjects participating in this program, SOLVD is the largest clinical heart failure study ever mounted. It is important to consider the design rationale of this program.

Double-Blind Method↗
PubMed1990

Effects of a vasopressin antagonist with combined antipressor and antiantidiuretic activities in rats with left ventricular dysfunction.

These experiments assessed the hemodynamic and aquaretic effects of an arginine vasopressin (AVP) antagonist with dual V1V2-receptor inhibiting properties in rats with congestive heart failure resulting from ischemic cardiomyopathy. The compound d(CH2)5-D-Tyr(Et)VAVP was used in these studies. Rats with limited or extensive myocardial infarcts (i.e., with less than 50% or greater than 66% necrosis of the left ventricular wall, respectively, induced by left coronary ligation) and sham-operated controls received the AVP antagonist (100 micrograms/kg i.v.) 4 weeks later. This agent produced an 18% increase in cardiac output (p less than 0.05) and 13% decrease in systemic vascular resistance in the severely damaged rats, both changes being significantly different from those seen in the normal controls or the rats with limited infarcts. All animals exhibited increases in urinary output of 4-10-fold over baseline. We conclude that the hemodynamic and renal effects of this agent are beneficial in animals with left ventricular dysfunction.

Animals↗
PubMed1994

Ventricular dysfunction in norepinephrine-induced cardiomyopathy.

Cardiac dysfunction resulting from norepinephrine-induced cardiomyopathy has not been fully investigated. This study evaluates acute and chronic changes in systolic and diastolic function at three levels of norepinephrine (NE)-induced injury. Rabbits were infused with saline or 2, 4, or 6 micrograms/kg/min NE for 90 min. Ventricular function was assessed immediately after infusion or at 48 hr using the isolated non-ejecting heart preparation. Hearts were perfused at 10 ml/min/g with Krebs-Henseleit buffer. After baseline measurements, hearts were perfused with NE (10(-10) to 10(-7) M). Steady state left ventricular pressure (LVP), +dP/dt, and -dP/dt were recorded at baseline and each NE concentration. NE infusion acutely depressed baseline LV systolic function. Decreases in LVP and +dP/dt were inversely related to dose of infused NE. By 48 hr, LVP and +dP/dt improved slightly in all NE groups but improvement was significant only in hearts from rabbits infused with 4 micrograms NE. Systolic function of hearts from animals infused with 6 micrograms NE remained depressed. Diastolic (-dP/dt) function was impaired following NE infusion when compared to saline treated hearts and did not improve within 48 hr. Although baseline function is depressed, myopathic hearts increased ventricular function the same amount as normal hearts at 10(-7) M NE. These findings demonstrate a) impairment in LV systolic and diastolic function acutely after NE infusion, b) improvement in systolic function within 48 hr, c) ability to increase contractility in response to NE is not impaired, and d) recovery of systolic function precedes improvement in diastolic function.

Animals↗
PubMed2003

Exercise training without ventricular remodeling in patients with moderate to severe left ventricular dysfunction early after acute myocardial infarction.

BACKGROUND: The purpose of this study was to determine whether or not patients with moderate to severe left ventricular (LV) dysfunction benefit from exercise training starting early after acute myocardial infarction (AMI) without deteriorating LV remodeling. METHODS: We investigated changes in exercise capacity and LV end-diastolic dimension (LVDd by two-dimensional echocardiography) before and after exercise training in 126 patients after AMI. Patients were divided into three groups according to LV ejection fraction (EF) at the beginning of exercise training: 74 patients with LVEF>/=45% (Group H), 35 patients with 35%</=LVEF<45% (Group M), and 17 patients with LVEF<35% (Group L). Exercise training was prescribed at a moderate intensity (50-60% of heart rate reserve or Karvonen's equation). Exercise capacity was assessed by peak work rate (WR) and peak oxygen uptake (VO(2)) by upright cardiopulmonary exercise test before and after 3 months of exercise training. LVDd was measured before and at 27+/-10 months of follow-up period. RESULTS: At the baseline, Group L had a significantly lower LVEF (H 55+/-7 vs. M 40+/-3 vs. L 30+/-3%, P<0.05), significantly greater LVDd (49+/-6 vs. 52+/-7 vs. 56+/-6 mm, P<0.05), and a higher incidence of anterior infarction (P<0.01) compared with Groups H and M, whereas there were no difference in age, sex, coronary risk factors, the incidence of multivessel disease, prior myocardial infarction, peak WR or peak VO(2) among the three groups. After 3 months of exercise training, exercise capacity increased significantly (all P<0.01) in all groups. The magnitudes of the increases in peak VO(2) (%Deltapeak VO(2): 18+/-20 vs. 15+/-19 vs. 18+/-17%, NS) and peak WR (%Deltapeak WR: 17+/-17 vs. 16+/-14 vs. 15+/-13%, NS) were similar among the three groups. In addition, there was no significant correlation between %Deltapeak VO(2) and baseline LVEF. No increase in LVDd was observed in any group at follow-up (H 48+/-5 to 49+/-4 mm vs. M 53+/-8 to 52+/-8 mm vs. L 57+/-5 to 57+/-7 mm, NS in each group). CONCLUSION: Patients with moderate to severe LV dysfunction benefit from exercise training starting early after AMI without deteriorating LV remodeling, with a similar magnitude of improvement in exercise capacity to that in patients with mild LV dysfunction.

Adult↗
PubMed2001

Left ventricular dysfunction and disturbed O(2)-utilization in stunned myocardium: influence of ischemic preconditioning.

OBJECTIVE: Myocardial dysfunction during postischemic reperfusion is frequently reported only in terms of left ventricular (LV) systolic properties. We additionally assessed diastolic properties, the cardiovascular tone and in particular, the relation between ventricular function and myocardial oxygen consumption. Moreover, these measures are investigated after cardioprotection via ischemic preconditioning (IP). However, this phenomenon is not fully understood, and therefore cardioprotective methods like ischemic preconditioning might provide only insufficient protection. METHODS: In a total of 17 isolated rabbit hearts, perfused with an erythrocyte suspension (Hct 30%), we investigated the effect of 20 min low-flow ischemia also on diastolic properties, coronary resistance and cardiac energetics (n=9). During control and 30 min after the onset of reperfusion, LV systolic function was assessed in terms of aortic flow, dP/dt(max) and the end-systolic pressure-volume relation (ESPVR). Early relaxation was evaluated via dP/dt(min) and diastolic properties were assessed via the end-diastolic pressure-volume relation (EDPVR), i.e. using the equation LVP(ed)=c.exp(m.LVV(ed)), where c equals the LVP(ed)-axis intercept and m equals LV stiffness. In addition, coronary resistance (R(cor)) and the pressure-volume area (PVA) were calculated. Total oxygen consumption (MVO(2)) was calculated as well as the contractile efficiency (E = inverse slope of the MVO(2)-PVA relation). In a second series (n=8) the effect of ischemic preconditioning (3 min no-flow and 8 min reperfusion before the 20 min low-flow ischemia) was tested. RESULTS: In the first series, systolic function was impaired during reperfusion: aortic flow to 32% of control, dP/dt(max) to 74% and the slope of ESPVR to 73%. Early relaxation in terms of dP/dt(min) decreased to 76%. The slope of the EDPVR was steeper in stunned myocardium with an increase of the ventricular stiffness (m increased from 3.2 to 4.1) and with an upward shift of the EDPVR (c from 0.6 to 2.4 mmHg). Coronary resistance was increased (from 0.9 to 1.4 mmHg/ml per min) and PVA was significantly decreased to 68%, whereas MVO(2) was not, indicating also a decrease in contractile efficiency E from 28 to 14%. In the second series, recovery of systolic function was significantly improved by IP compared with the first series (aortic flow 56% of preischemic control, dP/dt(max) to 91% and ESPVR to 78%). LV stiffness m was also slightly increased from 3.1 to 3.9 and again, c was elevated, indicating no beneficial effect for diastolic properties including dP/dt(min) (77%). But IP improved R(cor) significantly (from 0.9 to only 1.0 mmHg/ml per min) and efficiency E to 21% (from 27% during control). CONCLUSION: Brief episodes of ischemia not only induce systolic but also diastolic and vascular stunning at almost maintained MVO(2). The decreased contractile efficiency clearly indicates an impaired O(2)-utilization of the contractile apparatus. Ischemic preconditioning did not improve diastolic function during reperfusion, but it provided protection with respect to vascular stunning and myocardial energetics.

Animals↗
PubMed1995

ECG differentiation of idiopathic dilated cardiomyopathy from coronary artery disease with left ventricular dysfunction.

To elucidate electrocardiographic differences of dilated cardiomyopathy (DCM) and coronary artery disease (CAD) with left ventricular (LV) dysfunction, 12-lead electrocardiograms in 23 patients with DCM, 36 patients with CAD and LV dysfunction, and 63 normal subjects were analyzed. Abnormal Q waves were seen in 69% of CAD patients and in 26% of DCM patients. Abnormal Q waves in leads II, III, aVF, or V2-V4 were present in 61% of CAD patients compared with 4% of DCM patients (P < .001). The R wave in lead RV6 voltage in DCM was the highest among the three groups and correlated with the degree of LV dilatation. RV6 voltage in CAD was the lowest and decreased in proportion to the severity of the apical thallium-201 defect RV6 voltage of 15 mm or more was present in 78% of DCM patients compared with 11% of CAD patients (P < .001). The R waves in leads I, II, and III (RI, RII, RIII) were also low in DCM. Therefore, all voltage ratios of RV6/RI, RII, RIII were the highest in DCM. In particular, the ratio of RV6 over the maximum R wave in leads I, II, and III (RV6/Rmax) in DCM correlated with the degree of LV dilatation and inversely with ejection fraction. RV6/Rmax was significantly higher in the DCM group compared with the CAD and control groups (3.3 vs 1.2, 1.2, respectively; P < .001). This ratio of 3 or more was present in 61% of the DCM patients but in none of the CAD patients or normal subjects (P < .001).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiomyopathy, Dilated↗
PubMed1984

The systolic arterial pressure/end-systolic volume relationship in patients with severe left ventricular dysfunction.

Performance of the intact left ventricle is well-defined by the end-systolic pressure/end-systolic volume relationship that appears independent of preload and afterload. To determine whether noninvasive measurements of this relationship could distinguish normal from abnormal subjects, we evaluated the relationship between arterial systolic pressure (determined by cuff sphygnomanometry) and radionuclide estimates of end-systolic volume in 12 normal subjects and 24 patients with severe left ventricular dysfunction. Data were acquired at rest, after atropine injection, and then during at least three increments of arterial pressure (average total increase approximately 45 mm Hg) using phenylephrine. The relationship between peak-systolic pressure (SP) and end-systolic volume (ESV) was found to be linear in all subjects (r greater than or equal to 0.91). The slope of this line was steeper in normal subjects than in myopathic patients (73 +/- 21.7 vs 20.8 +/- 8.7 mm Hg/volume unit/m2, P less than 0.001) and the zero pressure intercept also was greater (49.8 +/- 30 mm Hg vs 27.1 +/- 44.2 mm Hg, P less than 0.01). Similarly, resting ejection fraction (EF) was greater in the normals (0.71 +/- 0.88 vs 0.21 +/- 0.07% P less than 0.001) and end-diastolic volume (EDV) was smaller (4.14 +/- 0.88 vs 6.58 +/- 0.65 volume units, P less than 0.01). Systolic pressure/end-systolic volume relationship determined by these noninvasive methods was linear in both patients with severely reduced cardiac function and normal control subjects, clearly distinguishing normal from severely impaired left ventricles.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Reversibility of severe left ventricular dysfunction due to doxorubicin cardiotoxicity. Report of three cases.

Doxorubicin is a potent anticancer agent effective in a wide range of malignancies, but its use is limited by dose-dependent late cardiotoxicity. Severe doxorubicin cardiotoxicity has been associated with a poor prognosis and a high mortality rate, and until recently has been thought to be irreversible. We describe the cases of three patients with well-documented severe left ventricular dysfunction due to doxorubicin who had complete clinical recovery with return of cardiac function to normal. Because severe doxorubicin cardiotoxicity is reversible in some patients, aggressive supportive therapy is warranted.

Adult↗
PubMed1994

Value of metabolic imaging with positron emission tomography for evaluating prognosis in patients with coronary artery disease and left ventricular dysfunction.

Patients with coronary artery disease (CAD) and severe left ventricular (LV) dysfunction have a high but variable annual mortality and some may benefit from myocardial revascularization. This study aimed to evaluate the prognostic value of positron emission tomography (PET), and its interrelation with the choice of medical therapy or revascularization for predicting survival and improvement in symptoms of heart failure in patients with CAD and LV dysfunction. Ninety-three consecutive patients with angiographic CAD and a mean LV ejection fraction of 0.25 who underwent cardiac PET studies for assessment of hypoperfused yet viable myocardium ("mismatch pattern") using N-13 ammonia and 18-F deoxyglucose were followed up for an average of 13.6 months. Fifty patients underwent medical treatment and 43 underwent revascularization. The Cox model analysis showed that the extent of mismatch had a negative effect (p = 0.02), whereas revascularization had a positive effect on survival (p = 0.04). The annual survival probability of patients with mismatch receiving medical therapy was lower than of those without mismatch (50 vs 92%, p = 0.007). Patients with mismatch who underwent revascularization had a higher survival rate than those treated medically (88 vs 50%, P = 0.03). The presence of mismatch also predicted improvement in heart failure symptoms after revascularization (p < 0.001). These results suggest that the presence of mismatch in patients with CAD and severe LV dysfunction is associated with poor annual survival with medical therapy. Revascularization in patients with PET mismatch appears to be associated with improved survival and heart failure symptoms.

Aged↗
PubMed2003

The impact of left ventricular dysfunction on cardiac donor transplant rates.

BACKGROUND: Because of the shortage of heart donors in the United States, efforts are necessary to maximize the yield of donor screening. The purpose of this study was to quantify the effects of left ventricular (LV) systolic dysfunction on heart donor use. METHODS: Using the California Transplant Donor Network database, the records of all potential organ donors screened between January 1997 and June 1998 were reviewed. After excluding subjects for whom family consent could not be obtained and subjects <13 or >or=60 years old, a study group of 223 potential heart donors was analyzed. The number of hearts not used because of LV dysfunction, coronary artery disease (CAD), valvular disease, and LV hypertrophy were quantified. A logistic regression model was developed to quantify the independent effect of LV dysfunction on donor use rates after adjustment for age, weight, and cause of death. RESULTS: Ninety-nine (44%) of the 223 potential donor hearts were not transplanted. Thirty-six of these hearts were not transplanted because of cardiac causes, primarily LV dysfunction (26 cases) and CAD (8 cases). The multivariable analysis showed that after adjusting for other donor variables, ejection fraction was the most significant predictor of non-use, with an odds ratio of 1.48 per 5-point decrease in ejection fraction. CONCLUSIONS: Left ventricular dysfunction is an important cause of failure to transplant adult donor hearts. Efforts to improve the yield of heart donor screening should focus on prevention or reversal of LV dysfunction.

Adult↗
PubMed1989

The effect of diabetes mellitus on prognosis and serial left ventricular function after acute myocardial infarction: contribution of both coronary disease and diastolic left ventricular dysfunction to the adverse prognosis. The MILIS Study Group.

Patients with diabetes mellitus experience a more adverse outcome after acute myocardial infarction compared with nondiabetic patients, although the mechanisms responsible for these findings are not clear. From the Multicenter Investigation of the Limitation of Infarct Size (MILIS) study, the course of acute infarction in 85 diabetic patients was compared with that in 415 nondiabetic patients, all of whom had serial assessments of left ventricular function. The diabetic patients experienced a more complicated in-hospital and postdischarge course than did the nondiabetic patients, including a higher incidence of postinfarction angina, infarct extension, heart failure and death, despite the development of a smaller infarct size and similar levels of left ventricular ejection fraction. Although diabetic patients had a worse profile of cardiovascular risk factors at the time of the index infarction, the increased incidence of adverse outcomes among them persisted despite adjustment for these baseline imbalances. Diabetic women had a poor baseline risk profile compared with the other groups categorized by gender and diabetic status, and experienced an almost twofold increase in cardiac mortality despite development of the smallest infarct size during the index event. The duration of diabetes and the use of insulin at the time of the index infarction were associated with a better in-hospital mortality rate, but the duration of diabetes did not exert a major influence on the outcome of the diabetic patients. The factors responsible for the increased incidence of adverse outcomes among diabetic patients may be related to an acceleration of the atherosclerotic process, diastolic left ventricular dysfunction associated with diabetic cardiomyopathy or other unidentified unfavorable processes.

Cardiovascular Diseases↗
PubMed1985

Acute myocardial infarction complicated by left ventricular dysfunction and respiratory failure. The effects of continuous positive airway pressure.

The cardiopulmonary effects of continuous positive airway pressure (CPAP) were studied in 14 patients with acute myocardial infarction complicated by circulatory and respiratory failure. Cardiac performance, lung mechanics, and gas exchange were assessed during 50 percent mechanical ventilatory support at end-expiratory airway pressure levels of 0, 5, 10, and 15 mm Hg. The increase in airway pressure resulted in significantly improved arterial blood oxygenation (p less than 0.001) and in a substantial reduction in the spontaneous respiratory effort (p less than 0.001). We observed a slight decrease in stroke volume index (p less than 0.05) with increasing airway pressure in patients who had moderate left ventricular dysfunction, and a trend of improvement (NS) in those who had severe pump failure. Relatively high levels of CPAP can be used to improve pulmonary function in patients with acute myocardial infarction and left ventricular failure. In fact, circulatory depression is less likely to occur when cardiac performance is poor.

Aged↗
PubMed1987

Left atrial abnormalities indicating diastolic ventricular dysfunction in cardiopathy of obesity.

Electrocardiograms and M-mode echocardiograms were evaluated in lean and obese patients, either normotensive or hypertensive, who were paired for mean arterial pressure, age, and sex. Electrocardiographic evidence of left atrial abnormalities (LAA) occurred more frequently (p less than 0.01) and left atrial size was greater in the obese than in the lean patients (p less than 0.01). The left atrial emptying index, an indicator of early diastolic ventricular function, was reduced in obese patients (p less than 0.01), most markedly in those with obesity-hypertension. The left atrial emptying index was reduced in obese patients with electrocardiographic LAA compared to obese patients without this electrocardiographic sign (p less than 0.02). A close correlation (r = 0.61, p less than 0.001) was obtained between the left atrial emptying index and atrial ECG abnormalities. These left atrial abnormalities in obesity and particularly in obesity-hypertension indicate diastolic ventricular dysfunction.

Adult↗
PubMed1987

Hemodynamic effects of the beta 1-adrenoceptor partial agonist xamoterol in relation to plasma norepinephrine levels during exercise in patients with left ventricular dysfunction.

A new cardioselective beta 1-adrenoceptor partial agonist, xamoterol, has been developed for the treatment of heart failure, especially that associated with ischemic heart disease. To investigate the hemodynamic effect of xamoterol in relation to sympathetic nervous activity, hemodynamic variables and plasma norepinephrine (NE) levels were measured at rest and during three graded bicycle exercise tests before and after a single intravenous dose of 0.15 mg/kg xamoterol in 10 patients with mild-to-moderate left ventricular dysfunction. Plasma NE increased with increasing grade of exercise and a linear correlation between plasma NE and heart rate was observed at four time points (at rest and three exercise levels) before and after xamoterol. After administration of xamoterol, the slope of the regression line of plasma NE-heart rate relation was significantly less steep than that before drug. Predose and postdose regression lines crossed at 440 pg/ml of plasma NE. Similar effects were observed on the plasma NE-cardiac index and plasma NE-systolic blood pressure relations (regression lines crossed at 380 and 530 pg/ml of plasma NE, respectively). Thus, xamoterol had a dual agonist-antagonist effect in relation to plasma NE, and the crossover point lay approximately between 400 pg/ml and 500 pg/ml. This level of plasma NE was achieved at a low exercise level and at a heart rate of about 100 beats/min. These results indicate that xamoterol has intrinsic sympathomimetic activity comparable to relatively low sympathetic activity (400 to 500 pg/ml of plasma NE) and therefore acts as a beta 1-agonist when sympathetic nervous activity is below this level and as an antagonist when sympathetic activity is above this level.

Adrenergic beta-Antagonists↗
PubMed2006

Relation of T-wave alternans to regional left ventricular dysfunction and eccentric hypertrophy secondary to coronary heart disease.

Left ventricular (LV) hypertrophy and structural disease are associated with exaggerated repolarization dispersion and risk for cardiac arrest. We hypothesized that T-wave alternans (TWA) from the electrocardiogram, reflecting proarrhythmic repolarization dispersion, would increase with extent of eccentric LV hypertrophy and vary spatially with the distribution of myocardial scar. We studied 28 patients with coronary disease, systolic dysfunction, and nonsustained ventricular tachycardia. On echocardiography, 21 patients had wall motion abnormalities and 20 had LV hypertrophy (mass index > or =100 g/m(2)). TWA magnitude (voltage of alternation), which was computed spectrally during ventricular stimulation, varied linearly with LV mass index (p = 0.003). Spatially, positive TWA (magnitude > or =1.9 microV) in orthogonal electrocardiographic axes overlaid scar or wall motion abnormalities in corresponding echocardiographic segments (p <0.05 in x and y axes). After a follow-up of 35 +/- 13 months, positive TWA predicted the combined end point of death or sustained ventricular arrhythmias in all patients (p = 0.025), with a trend for those with echocardiographic LV hypertrophy (p = 0.058). In conclusion, in patients with systolic dysfunction due to coronary artery disease, TWA may indicate arrhythmic contributions from regional myocardial scar and eccentric LV hypertrophy.

Aged↗
PubMed2000

Evaluation of brain natriuretic peptide as marker of left ventricular dysfunction and hypertrophy in the population.

OBJECTIVE: To evaluate brain natriuretic peptide (BNP) as marker of left ventricular (LV) dysfunction and hypertrophy in a population-based sample of 610 middle-aged subjects (50-67 years) who were further characterized with respect to hemodynamic and anthropometric parameters and by echocardiography. RESULTS: Left ventricular (LV) systolic function, LV mass-index, age, gender, heart rate, and medication with beta adrenergic receptor blockers were significant and independently correlated with BNP (multivariate analysis, P < 0.05 each). As compared to subjects with normal LV function and mass-index (control), subjects with LV dysfunction (LV fractional shortening < 28%) or hypertrophy (LV mass-index > 110 g/m2 in women and > 134 g/m2 in men) were characterized by increased BNP. The increase in BNP associated with LV hypertrophy (n = 69, +101% versus control, P < 0.0001) was similar in magnitude to that associated with LV dysfunction (n = 39, +98% versus control, P < 0.03). These increases were markedly exceeded in subjects with severe LV dysfunction (n = 11, LV fractional shortening < 22%, BNP +197% versus control, P < 0.01), particularly in the presence of concomitant hypertrophy (n = 7, +227%, P < 0.01). The predictive values of BNP varied considerably with the degree of LV dysfunction and the presence or absence of concomitant LV hypertrophy. With 0.81, the highest area under the receiver operator characteristic curve was obtained for the detection of severe LV dysfunction and concomitant hypertrophy and sensitivity, specificity, positive and negative predictive value for this condition were 71, 86, 7 and 99.5%, respectively, for a cut-off of 34 pg/ml. CONCLUSIONS: The current study provides new insight into regulation and diagnostic value of BNP in middle-aged subjects and demonstrates important independent effects of LV function and mass upon BNP plasma concentrations. Although measurement of BNP cannot be recommended for the detection of marginally impaired LV function in the population, it may be helpful to suggest or exclude severe LV dysfunction with concomitant hypertrophy.

Analysis of Variance↗
PubMed1992

Cardiodepressant effects of mexiletine in patients with severe left ventricular dysfunction.

Mexiletine is thought to exert minimal negative inotropic actions, but its effects have not been evaluated in patients with severe congestive heart failure. The haemodynamic response to an oral loading dose of mexiletine (400 mg) was assessed in 20 patients with severe chronic heart failure. Mexiletine caused marked haemodynamic deterioration, with stroke work index decreasing in 18 of the patients. Two hours after mexiletine, mean cardiac and stroke work indexes decreased by 15% and 25%, respectively (both P less than 0.001), while heart rate and systemic vascular resistance increased by 10% and 20%, respectively (both P less than 0.05). Simultaneously, left ventricular filling pressure and right atrial pressure increased by 37% and 36%, respectively (both P less than 0.001), but mean arterial pressure did not change. Furthermore, clinical deterioration, with onset of dyspnoea at rest, developed in five patients at the time of peak haemodynamic effect. Plasma mexiletine concentrations were within the accepted therapeutic range of 0.5 to 2.0 micrograms.ml-1 in all but two of the patients. Nevertheless, the plasma concentration was an important determinant of haemodynamic effect. The stroke work index decreased by 38% in the patients with a mexiletine level above the median value of 1.3 micrograms.ml-1 (range 25 to 56%), but only 13% (range 15 to 43) in patients with lower plasma concentrations. In conclusion, although mexiletine may cause cardiodepressant effects in any patient with severe left ventricular dysfunction, dosing which results in a high (but still therapeutic) plasma level is more likely to cause haemodynamic deterioration.

Adult↗
PubMed2001

Utility of B-natriuretic peptide as a rapid, point-of-care test for screening patients undergoing echocardiography to determine left ventricular dysfunction.

BACKGROUND: Although echocardiography is an important tool for making the diagnosis of left ventricular (LV) dysfunction, the cost of this procedure limits its use as a routine screening tool for this purpose. Brain natriuretic peptide (BNP) accurately reflects ventricular pressure, and preliminary studies have found it to be highly sensitive and highly specific in diagnosing congestive heart failure in the emergency department. We hypothesized that BNP might therefore be useful as a screening tool before echocardiography in patients with suspected LV dysfunction. METHODS: Subjects included patients referred for echocardiography to evaluate the presence or absence of LV dysfunction. Patients with known LV dysfunction were excluded from analysis. BNP was measured by a point-of-care immunoassay (Biosite Diagnostics, San Diego, Calif). The results of BNP levels were blinded from cardiologists making the assessment of LV function. Patients were divided into those with normal ventricular function, abnormal systolic ventricular function, abnormal diastolic function, and evidence of both systolic and diastolic dysfunction. RESULTS: Two hundred patients in whom LV function was unknown were studied. In the 105 patients (53%) whose ventricular function was subsequently determined to be normal by echocardiography, BNP levels averaged 37 +/- 6 pg/mL. This was significantly less than in those patients with either ultimate diastolic dysfunction (BNP 391 +/- 89 pg/mL (P <.001) or systolic dysfunction (BNP 572 +/- 115 pg/mL (P <.001). A receiver-operator characteristic curve showing the sensitivity and specificity of BNP against the echocardiography diagnosis revealed the area under the curve (accuracy) was 0.95. At a BNP level of 75 pg/mL was 98% specific for detecting the presence or absence of LV dysfunction by echocardiography. CONCLUSIONS: A simple, rapid test for BNP, which can be performed at the bedside or in the clinic, can reliably predict the presence or absence of LV dysfunction on echocardiogram. The data indicate that BNP may be an excellent screening tool for LV dysfunction and may, in fact, preclude the need for echocardiography in many patients.

Aged↗