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PubMed1999

Neurohumoral prediction of benefit from carvedilol in ischemic left ventricular dysfunction. Australia-New Zealand Heart Failure Group.

BACKGROUND: Plasma neurohormones were analyzed for prediction of adverse outcomes and response to treatment in 415 patients with ischemic left ventricular dysfunction randomly assigned to receive carvedilol or placebo. METHODS AND RESULTS: Atrial natriuretic peptide, brain natriuretic peptide (BNP), or norepinephrine (NE) levels above the group median were associated with increased mortality rates and heart failure. On multivariate analysis, both BNP and NE interacted with treatment to predict death or heart failure independent of age, New York Heart Association class, and left ventricular ejection fraction. For placebo, supramedian levels of BNP were associated with 3-fold the mortality rate of inframedian levels (20/104; 19% vs 6/99; 6%; P<0.01). For carvedilol, mortality rate was comparable in these 2 subgroups (12/109; 11% vs 8/94; 9%; NS). Corresponding rates for heart failure were 29/104 (28%) versus 3/99 (3%; P<0.001) for placebo and 16/109 (15%) versus 7/94 (7%; NS) for carvedilol. High NE levels did not predict additional benefit from carvedilol, which significantly reduced heart failure admissions only in those with NE levels below the median (13.1% to 4. 0%; P<0.01). In the 23% of the study population with supramedian BNP but inframedian levels of NE, carvedilol reduced hospital admission with heart failure by >90% (P<0.001). CONCLUSIONS: Carvedilol reduced mortality rates and heart failure in those with higher pretreatment BNP levels but lesser activation of plasma NE. Neurohumoral profiling may guide introduction of beta-blockade in heart failure.

Arginine Vasopressin↗

PubMed1988

Right ventricular dysfunction in multiple trauma victims.

We studied 17 victims of multiple trauma and found that right ventricular function can be reliably monitored at the bedside using the thermodilution method. In addition, we noted that right ventricular dysfunction occurred early in victims of major trauma without affecting the left ventricular function. If right ventricular function does not improve, the patient is likely to die. Further studies are needed to determine if early intervention aimed at improving right ventricular function can improve survival.

Adolescent↗

PubMed1983

Selective right ventricular dysfunction after coronary artery bypass grafting.

Preoperative and postoperative right (RVEF) and left ventricular ejection fractions (LVEF) were studied by means of radionuclide techniques in 15 patients undergoing coronary bypass operations. Three of them, all with right coronary artery lesions, had postoperative depression of RVEF without concomitant decrease in LVEF. In contrast to those with left ventricular dysfunction, the patients with selective RVEF depression did not have significant elevation of myocardial injury index calculated from creatine kinase isoenzyme (CK-MB) curves.

Cardiac Output↗

PubMed2006

Relations among renal function, risk of sudden cardiac death, and benefit of the implanted cardiac defibrillator in patients with ischemic left ventricular dysfunction.

Implanted cardioverter defibrillator therapy has been shown to be associated with a significant reduction in the risk of sudden cardiac death (SCD) in patients with ischemic left ventricular dysfunction. However, data on the relation between renal function and SCD in this population are limited, and the effect of renal dysfunction on the implanted cardioverter defibrillator benefit has not been determined. We performed a retrospective analysis of the outcome associated with renal dysfunction, as determined by the estimated glomerular filtration rate (eGFR), in patients enrolled in the Multicenter Automatic Defibrillator Implantation Trial-II. Multivariate analysis in conventionally treated patients showed that for each 10-U reduction in eGFR, the risk of all-cause mortality and SCD increased by 16% (p = 0.005) and 17% (p = 0.03), respectively. Defibrillator therapy was associated with a survival benefit in each eGFR category of > or = 35 ml/min/1.73 m2 (overall risk reduction for all-cause mortality 32%, p = 0.01 and for SCD 66%, p < 0.001). However, no implanted cardioverter defibrillator benefit was shown among patients with an eGFR < 35 ml/min/1.73 m2 (all-cause mortality hazard ratio 1.09, p = 0.84; SCD hazard ratio 0.95, p = 0.95). In conclusion, in patients with high-risk cardiac disease enrolled in the Multicenter Automatic Defibrillator Implantation Trial-II, a significant increase was found in the risk of SCD with declining renal function. Defibrillator therapy was associated with a significant survival benefit among the study patients with mild to moderate or no renal disease, but no benefit was shown among patients with more advanced renal dysfunction.

Aged↗

PubMed1995

Cardiorespiratory reflex control in rats with left ventricular dysfunction.

Patients with heart failure exhibit a neurohumoral excitatory state and abnormal baroreflex control of the cardiovascular system. We determined whether arterial baroreflexes are impaired during left ventricular dysfunction (LVD) caused by chronic myocardial infarction in the absence of congestive heart failure and whether abnormal central mechanisms contribute to this impairment. Baroreceptors were stimulated in anesthetized rats with and without LVD by increasing arterial pressure with phenylephrine. Lumbar sympathetic nerve and phrenic nerve activity as well as heart rate were recorded. Rats were divided into different groups based on infarct size. Rats with moderate LVD showed impaired baroreflex control of sympathetic, ventilatory, and heart rate responses. Baroreflex gains were inversely related to the size of the infarct. The central gain for sympathetic nerve activity, obtained by using electrical stimulation of the aortic depressor nerve, also was impaired. Baroreflex control of the cardiorespiratory system is thus impaired in rats with moderate LVD in the absence of congestive heart failure. The attenuated baroreflexes are likely due to abnormal afferent mechanisms, although central mechanisms contribute to the impaired barosympathetic reflex.

Afferent Pathways↗

PubMed2005

Off pump coronary artery bypass surgery for significant left ventricular dysfunction: safety, feasibility, and trends in methodology over time--an early experience.

OBJECTIVE: To examine the safety and applicability of off pump coronary artery bypass surgery (OPCAB) in patients with significant left ventricular dysfunction and to discuss the clinical implications for the surgical methods. DESIGN: Retrospective study. SETTING: Tertiary care university affiliated referral centre. PARTICIPANTS: 353 consecutive patients with preoperative left ventricular ejection fraction < or = 35% who underwent coronary artery bypass over a three year period. MAIN OUTCOME MEASURES: Postoperative morbidity and mortality. METHODS: 144 patients operated by OPCAB were compared with 209 patients operated by conventional coronary artery bypass. Multivariate and univariate analyses were performed on the pre- and postoperative variables to predict risk factors associated with hospital morbidity and mortality. RESULTS: Patients in the OPCAB group were more likely to be women and to have congestive heart failure, chronic obstructive pulmonary disease, hypertension, and diabetes; patients in the on pump group were more likely to have had a recent myocardial infarction and to have more severe angina pectoris and an urgent/emergent status. The groups did not differ significantly in length of stay, major postoperative complication rates, or mortality. Comparison of the impact of the procedures on surgical methods over time showed an increase in the use of OPCAB (13% to 67%), without any impact on morbidity or mortality. CONCLUSIONS: OPCAB is feasible and applicable for patients with depressed left ventricular function. This high risk group can potentially benefit from the off pump approach.

Aged↗

PubMed2006

Biomarker-based strategy for screening right ventricular dysfunction in patients with non-massive pulmonary embolism.

OBJECTIVE: To evaluate the usefulness of B-type natriuretic peptide and troponin I measurements in predicting right ventricular dysfunction (RVD) in non-massive pulmonary embolism. DESIGN: Prospective observational study. SETTING: University-affiliated emergency unit, cardiology and pneumology departments. PATIENTS: Sixty-seven patients admitted because of acute pulmonary embolism, without shock on admission, completed the study. INTERVENTIONS: Blood samples and echocardiography were obtained on admission for subsequent and independent assessment of B-type natriuretic peptide (BNP) and troponin I levels as well as RVD. MEASUREMENTS AND RESULTS: Echocardiographic RVD was diagnosed in 36 patients and was severe in 13 on admission. BNP and troponin I levels were higher in patients with RVD than in those with no RVD [62 (27-105) vs. 431 (289-556) pg/ml for BNP, p<0.001; 0.01 (0-0.09) vs. 0.16 (0.03-0.32) microg/l for troponin I, p=0.005]. The area under the receiving operating characteristic curve (AUC) for diagnosing RVD was 0.93 for BNP and 0.72 for troponin I. The troponin I level increased further when RVD was severe, compared with moderate, and the AUC was 0.91 for identifying severe RVD. Diagnoses of RVD and severe RVD were ruled out by BNP 100 pg/ml and troponin I >0.10 microg/l. CONCLUSION: In hemodynamically stable pulmonary embolism, BNP/troponin I measurement is helpful on admission, especially for ruling out RVD, i.e. patients with in-hospital high-risk.

Aged↗

PubMed1996

Economic aspects of treatment with captopril for patients with asymptomatic left ventricular dysfunction in The Netherlands.

OBJECTIVE: To estimate the costs and effects of preventive treatment with captopril compared with the current treatment policy in patients with asymptomatic left ventricular dysfunction after a myocardial infarction. METHODS: Estimates of effects are based on the results of the SAVE trial. Costs are estimated on the basis of current treatment patterns in four Dutch hospitals. All knowledge is incorporated in a mathematical model extrapolating the SAVE results to 20 years. RESULTS AND CONCLUSIONS: Captopril treatment is expected to increase survival at certain costs. The average additional costs per patient are estimated at DF1 2,491 in 4 years and at DF1 8,723 in 20 years of treatment. Costs per additional survivor after 4 years are estimated at DF1 69,126. After extrapolation of the results of the SAVE trial to 20 years, costs per life-year gained can be estimated at DF1 15,799. From univariate sensitivity analysis it appears that the results are highly sensitive for the costs of treatment with captopril and the occurrence and prevention of clinical heart failure. Varying all estimates randomly between upper and lower limits-in 5,000 simulations-an estimate of costs per life-year gained of DF1 15,729 is made for 20 years of treatment, with 95% of all estimates between DF10 and DF1 50, 000. On a national level, undiscounted costs are expected to increase up to approximately DF1 42 million annually during the first 40 years after introduction of the preventative strategy.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed2003

Diuretic use, progressive heart failure, and death in patients in the Studies Of Left Ventricular Dysfunction (SOLVD).

OBJECTIVES: We sought to determine whether non-potassium-sparing diuretics (PSDs) in the absence of a PSD may result in progressive heart failure (HF). BACKGROUND: Angiotensin-converting enzyme (ACE) inhibitors incompletely suppress ACE activity in HF patients. Furthermore, non-PSDs are activators of aldosterone secretion. We reasoned that non-PSDs, in the absence of a PSD, might result in progressive HF. METHODS: In the 6,797 patients in the Studies Of Left Ventricular Dysfunction (SOLVD), we compared the risk of hospitalization for, or death from, HF between those taking a PSD and those who were not, adjusting for known covariates. RESULTS: The risk of hospitalization from worsening HF in those taking a PSD relative to those taking only a non-PSD was 0.74 (95% confidence interval [CI] 0.55 to 0.99; p = 0.047). The relative risk for cardiovascular death was 0.74 (95% CI 0.59 to 0.93; p = 0.011), for death from all causes 0.73 (95% CI 0.59 to 0.90; p = 0.004), and for hospitalization for, or death from, HF 0.75 (95% CI 0.58 to 0.97; p = 0.030). Compared with patients not taking any diuretic, the risk of hospitalization or death due to worsening HF in patients taking non-PSDs alone was significantly increased (risk ratio [RR] = 1.31, 95% CI 1.09 to 1.57; p = 0.0004); this was not observed in patients taking PSDs with or without a non-PSD (RR = 0.99, 95% CI 0.76 to 1.30; p = 0.95). CONCLUSIONS: The use of PSDs in HF patients is associated with a reduced risk of death from, or hospitalization for, progressive HF or all-cause or cardiovascular death, compared with patients taking only a non-PSD.

Aged↗

PubMed1995

Ability of the no-reflow phenomenon during an acute myocardial infarction to predict left ventricular dysfunction at one-month follow-up.

Despite angiographically successful opening of an infarct-related vessel within a 6-hour time frame, some patients do not recover left ventricular regional wall function in the infarct zone after an acute myocardial infarction (AMI). Recent evidence suggests that this finding is due to the no-reflow phenomenon, or failure to recover tissue perfusion despite patient epicardial arteries. We performed myocardial contrast echocardiography to assess tissue perfusion before and after opening of an infarct-related artery. Coronary angiograms, regional wall motion scoring, and myocardial contrast enhancement were graded by 3 observers. Of 24 patients with AMI, 7 (29%) failed to recover tissue perfusion in > or = 1 region of myocardium. Of 106 regions subtended by the infarct-related artery, 16 (15%), 43 (41%), and 47 (44%) regions had no-reflow, partial, or normal flow, respectively, after arterial patency was established. There was a spectrum of reperfusion patterns ranging from no-reflow to normal perfusion. One-month follow-up angiographic and myocardial contrast echocardiographic studies were performed in 12 of the 24 patients. At 1 month, all segments of myocardium that had immediate normal perfusion had regained normal wall motion. In contrast, 17 segments that had partial or no-reflow were identified. Of these 17, 3 regained normal function, 10 segments were hypokinetic, and 4 segments were akinetic. We conclude that myocardial contrast echocardiography can be used to identify the no-reflow phenomenon in up to 29% of patients with AMI. Additionally, we found that the immediate-reflow pattern can predict degree of left ventricular dysfunction at 1-month follow-up.

Adult↗

PubMed2006

Fatal case of amiodarone-induced acute respiratory distress syndrome in a patient with severe left ventricular dysfunction due to extensive anterior acute myocardial infarction.

We here report a case of 71-year-old man with acute extensive anterior myocardial infarction, who was complicated with ventricular tachycardia (VT) even after successful percutaneous coronary intervention. As intravenous administration of nifekalant terminated VT, we started oral administration of amiodarone (day 1). We gave 400 mg of amiodarone a day for the first week and 200 mg a day from the second week. The patient was stable with normoxia by day 20, in spite of pulmonary congestion-like infiltrates on chest X-ray. On day 21, he was complicated with acute respiratory distress syndrome. Immediate discontinuance of amiodarone and high-dose pulse glucocorticoid therapy with intubation slightly improved the infiltrations on chest X-ray. However, glucocorticoid therapy induced hyperglycemia with an increase in plasma osmolality, complicated with hypoalbuminemia, and gastrointestinal bleeding. Despite treatment with a large amount of saline, high-doses of catecholamines, and blood transfusion, the patient died on day 28. It is sometimes difficult to diagnose congestive heart failure or amiodarone-induced pulmonary infiltrates in patients with severe left ventricular dysfunction.

Aged↗

PubMed2006

Troponin I as a marker of right ventricular dysfunction and severity of pulmonary embolism.

BACKGROUND: Cardiac troponin I (cTnI) is a specific marker which allows detection of minor myocardial cell damage. In patients with severe pulmonary embolism (PE), the rise in pulmonary artery pressure can lead to progressive right ventricular dysfunction (RVD), and clinical studies have demonstrated the presence of ischemia and even right ventricular infarction. Our aims were to determine the prevalence and diagnostic utility of cTnI in identifying patients with RVD and to ascertain whether it correlates with severity of PE. METHODS: We studied 77 patients with PE diagnosed by pulmonary angiography, ventilation-perfusion lung scan, spiral computed tomography scan or a combination of abnormal echocardiogram with clinical presentation suggestive of PE or with positive subsidiary exams (d-dimers, venous Doppler of the lower limbs, ECG, blood gas analysis). We further classified the PE according to the European Society of Cardiology severity levels, the PE being: 1) massive, if there was shock and/or hypotension; 2) submassive, if we found right ventricular hypokinesis on the echocardiogram; and 3) non-massive, in the remaining cases. We considered the highest cTnI serum value from the admission to 24 hours and a normal value of < 0.10 ng/ml. RESULTS: Among the 60 patients with cTnI measurements, 42 had elevated values. Among those with RVD, 26 (81.3%) had increased cTnI levels and only 14 (35%) with elevated cTnI values did not have RVD, indicating that positive cTnI tests were significantly associated with RVD (p = 0.038). Patients with positive cTnI tests had earlier onset of symptoms (24.0 vs. 144.0 hours, p=0.02), higher prevalence of emboli in proximal vessels (pulmonary trunk and right or left main pulmonary arteries) (OR = 12, CI= 1.6-88.7), and received more thrombolytic therapy (OR = 5.4, CI = 1.1-26.8) than those with normal cTnI tests. cTnI levels were higher among patients with submassive PE (median: 0.77 ng/ml) and lower in those with non-massive PE (0.08 mg/ml, p < 0.05). CONCLUSIONS: Around 70% of patients with PE have elevated cTnI values and this test is significantly associated with RVD. cTnI measurements provide additional information in the evaluation of patients with PE by identifying more severe cases and those at increased risk of hemodynamic deterioration, who can benefit from more aggressive therapeutic strategies.

Biomarkers↗

PubMed1995

Efficacy and safety of nisoldipine coat core in the management of angina pectoris, systemic hypertension, and ischemic ventricular dysfunction.

The effects of the long-acting dihydropyridine calcium antagonist nisoldipine coat core (CC) have been investigated in > 3,500 patients with angina pectoris, hypertension, and ischemic ventricular dysfunction. In patients with angina pectoris, nisoldipine CC improved total treadmill exercise duration (p = 0.027), delayed the onset of angina pectoris (p = 0.009), and increased time to exercise-induced ST-segment depression (p = 0.061). In general, nisoldipine 20-40 mg was effective, and the dose-response curve flattened thereafter. In patients with hypertension, 10-40 mg once daily as monotherapy reduced blood pressure (p < 0.05), with a fall in diastolic pressure of > or = 10 mm Hg or a final diastolic pressure of < 90 mm Hg in 35-63% of patients. In most patients followed for a year, nisoldipine CC was continued as monotherapy. Efficacy was similar in patients < 65 and > 65 years of age. In the Doppler Flow and Echocardiography in Functional Cardiac Insufficiency: Assessment of Nisoldipine Therapy (DEFIANT-I) study of patients recovering from myocardial infarction, nisoldipine CC had a salutary effect on diastolic ventricular function, with a higher transmitral early filling velocity and shorter isovolumic relaxation time than in patients receiving placebo. Bicycle exercise capacity was greater (by 12 W; 95% confidence interval, 0.8-23.3) and exercise-induced ischemia occurred less frequently. The nisoldipine CC data pool (3,679 patients) showed that the drug was well tolerated with a low incidence of side effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗

PubMed2000

Senescent ventricular dysfunction: issues related to cardiopulmonary bypass.

The mean age of the open-heart surgical patient is increasing every year. Therefore, it is logical to define the aging-related changes in cardiovascular function. This study set forth to define the major molecular and performance alterations that occur in the left ventricle related to advanced aging or senescence. In the human, vascular pathologies usually accompany left ventricular dysfunction. The aim of this study was to associate the altered left ventricular mechanics with molecular pathways in mice who lacked these associated vascular pathologies. This study compared the left ventricular function of two groups of mice (N = 20 each), 6 months old and 16 months old (senescent). The mice were anesthetized with urethane and alpha-chloralose, and a Millar 1.4 Fr. conductance micromanometer catheter was placed into the left ventricle for acquisition of pressure-volume loops. Heart tissues were collected immediately for analysis of cGMP concentrations. The cardiac index, preload recruitable stroke work, and the slope (Ees) of the end-systolic pressure volume relationship were significantly less in the senescent group compared to the young mice. It was concluded that the aged heart has significantly reduced systolic and diastolic dysfunction compared to the young heart function and that this dysfunction may be related to pathways leading to increased myocardial cGMP concentrations.

Age Factors↗

PubMed2002

Pulmonary hypertension secondary to left ventricular dysfunction: the role of nitric oxide and endothelin-1 in the control of pulmonary vascular tone.

1. Using an in vivo model of pulmonary hypertension (PHT) secondary to left ventricular dysfunction (LVD), the pulmonary arterial response to the nitric oxide synthase (NOS) blocker L-NAME (30 micromol.min(-1) i.v.) and the subsequent responses to cumulatively administered endothelin-1 (ET-1) (0.001 -- 4 nmol.kg(-1) i.v.) or big ET-1 (0.1 -- 2.0 nmol.kg(-1) i.v.) were studied. Additionally, the effect of the non-selective ET-1 receptor antagonist, SB209670, was investigated. 2. Eight weeks after coronary artery ligation or sham operation, rabbits demonstrated increased mean pulmonary arterial pressure (PAP) accompanied by right ventricular hypertrophy. 3. Blockade of NOS caused a greater increase in basal PAP (increased by 7.7 +/- 1.1 mmHg c.f. 3.8 +/- 1.0 mmHg in controls, P<0.05) and uncovered a greater pulmonary pressor response to exogenous ET-1 in rabbits with PHT (increased by 10.2 +/- 2.3 mmHg c.f. 4.9 +/- 1.0 mmHg in controls, P<0.05). 4. Big ET-1 evoked a pulmonary pressor effect, in both groups of rabbits, that was increased following blockade of NOS and was more potent in rabbits with PHT. 5. The non-selective ET-1 receptor antagonist, SB209670, reduced basal PAP (from 16.9 mmHg to 15.9 mmHg, P < 0.05) in rabbits with PHT and blocked the response to ET-1 in the presence of L-NAME. 6. In conclusion, the results demonstrate that basal NO activity masks a pulmonary pressor response to exogenously administered ET-1. An increased responsiveness to ET-1 was shown in the pulmonary arterial bed of rabbits with PHT secondary to LVD, implicating a pathophysiological role for ET-1 in this model.

Animals↗

PubMed1989

Hemodynamic effects of dilevalol in patients with systemic hypertension and left ventricular dysfunction.

Hemodynamic and left ventricular function parameters were measured in patients with mild to moderate hypertension and compromised left ventricular function who were given dilevalol, an antihypertensive agent with selective beta 2-agonism and nonselective beta-antagonist activity. After a 2- to 3-week placebo washout period, 9 patients were given dilevalol titrated upward from 100 to 600 mg twice daily over a 7-week period to achieve a supine diastolic blood pressure of less than 90 mm Hg with a decrease of greater than or equal to 10 mm Hg from baseline. Multigated radionuclide ventriculography and systolic and diastolic time intervals were performed after the pretreatment placebo washout, at the end of 2 weeks' maintenance dosing, and after a 7- to 10-day post-treatment discontinuation and placebo washout period. At an average daily dose of dilevalol, 444 mg, heart rate at rest decreased significantly (p less than 0.01) during treatment and increased during post-treatment placebo. Systolic and diastolic blood pressures at rest decreased significantly (p less than 0.01) during treatment and increased during post-treatment placebo. At maximal exercise, changes in blood pressure and heart rate were significantly blunted (p less than 0.05) during treatment. Ejection fraction at rest increased significantly (p less than 0.01) during treatment, with no significant change occurring during exercise, and decreased during post-treatment placebo. Preejection period decreased significantly during treatment (p less than 0.005) and increased during post-treatment placebo.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1992

Is the morphology of ventricular premature beats a marker for left ventricular dysfunction?

The morphology of ventricular premature beats has been described as a marker for the presence or absence of myocardial disease. Furthermore, the premature beat has been reported to be a potential marker for a dilated and hypokinetic left ventricle. To verify this previously tested hypothesis, 37 healthy patients with ventricular premature beats on an electrocardiogram (ECG), Holter monitor ECG, or a stress test ECG were classified according to the ventricular premature beat morphology. Group 1 had ventricular premature beat QRS complexes with a smooth contour or with narrow (less than 40 msec) notching. Group 2 had ventricular premature beats with broad (greater than 40 msec) notching or shelves. All of these patients had normal or borderline normal ECGs and normal multiple-gated acquisition (MUGA) scans. Nine patients had type 1 ventricular premature beats, 20 patients had type II ventricular premature beats, and eight patients had both type I and type II ventricular premature beats. We conclude that the presence of group 2 ventricular premature beats is so frequent in patients with normal left ventricular ejection fractions that the use of this marker in identifying abnormal left ventricular function is suspect.

Adult↗

PubMed1990

[Pulmo cardialis: effect of inhaled bronchodilators on airway resistance of acute left ventricular dysfunction].

Disturbance of left ventricular function leads to an impairment of ventilation: airway resistance increases, while pulmonary compliance is reduced. We therefore studied the effect of inhalable bronchodilators (Fenoterol, Ipratropium bromide) on oscillatory airway resistance in 16 patients with an acute left heart failure. The results show that the resistance can be significantly reduced to normal values by the bronchodilators. Fenoterol has the greatest spasmolytic potency, but Ipratropium bromide is also effective. Recompensation of left heart function alone does not lead to comparable acute effects on airway resistance. The possibility of immediate improvement of ventilation through the use of inhalable bronchodilators should therefore be considered in the treatment of acute left heart failure.

Airway Resistance↗