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 TOP Article appraised Structured abstractCommentary by N. M....References |
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Structured abstract |
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TOPArticle appraisedStructured abstractCommentary by N. M....References |
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Design: Prospective, non-randomized, non-blinded trial. Patients, physicians, and nurses were aware of treatment regimens.
Setting: Cardiac Intensive Care Unit at the Cleveland Clinic Foundation from August 1, 2000 to May 15, 2002.
Patients: 29 consecutive patients met the inclusion criteria for the study. Four patients had hypotension and were excluded. Twenty-five patients began the study. One patient underwent aortic valve replacement before the 24-hr time point and was included in all the analyses except the 24-hr subgroup analysis. The inclusion criteria were: admission to an intensive care unit for invasive hemodynamic monitoring of heart failure; depressed left ventricular function (LVEF 
35%); severe aortic stenosis (aortic valve area = 1 cm2 on echocardiography); and a depressed cardiac index (2.2 L·min–1·m–2), as determined by the Fick method. The only exclusion criteria was hypotension, defined as either the need for iv vasopressor agents or a mean systemic arterial pressure (MAP) below 60 mmHg.
Intervention: All patients underwent continuous electrocardiogram (ECG) and invasive hemodynamic monitoring with pulmonary-artery catheter and arterial catheters. Heart rate, blood pressure, ECG findings, and cardiac hemodynamic variables were recorded at baseline. Nitroprusside was titrated to maintain a MAP between 60 and 70 mmHg; the exact dose was determined by the cardiologist. Nitroprusside was started at a dose of 14 ± 10 µg·min–1 (mean ± standard deviation or 0.2 ± 0.14 µg·kg–1·min–1 for 70-kg subjects), increased to 103 ± 67 µg·min–1 (or 1.47 ± 0.96 µg·kg–1·min–1 for 70-kg subjects) after six hours and further increased to 128 ± 96 µg·min–1 (or 1.83 ± 1.37 µg·kg–1·min–1) after 24 hr. After six and 24 hr of nitro-prusside infusion, heart rate, blood pressure, and cardiac hemodynamic variables were again recorded. All echocardiographic data was obtained by an experienced sonographer and read by a blinded experienced cardiologist. Patients were stratified by aortic valve gradient pressures into low-gradient (mean gradient; 30 mmHg, n = 11) and high-gradient (mean gradient; > 30 mmHg, n = 13) groups.
Main outcomes: The effect of nitroprusside on the cardiac index was the primary end-point. Secondary end-points included heart rate, MAP, pulmonary-capillary wedge pressure, systemic vascular resistance, and stroke volume. Recorded adverse events were hypotension (MAP < 60 mmHg), angina, evidence of new ischemia on ECG, acute renal failure, dyspnea, or arrhythmias.
Main results: The group mean ± standard deviation baseline LVEF was 21 ± 8%, aortic valve area 0.6 ± 0.2 cm2, cardiac index 1.60 ± 0.35 L·min–1·m–2, with peak and mean aortic valve pressure gradients of 65 ± 37 and 39 ± 23 mmHg. The cardiac index increased to 2.22 ± 0.44 L·min–1·m–2 at six hours (P < 0.001) and to 2.52 ± 0.55 L·min–1·m–2 at 24 hr (P < 0.001). Compared to baseline, there was a significant decrease in MAP, pulmonary capillary wedge pressure, pulmonary vascular resistance, pulmonary artery systolic pressure, and systemic vascular resistance at six and 24 hr. Right ventricular stroke volume had significantly increased at six and 24 hr. Heart rate did not change. There were similar increases in cardiac output with and without coronary artery disease, significant mitral regurgitation, and high vs low grade aortic stenosis. In a subgroup of six patients, nitroprusside significantly (P = 0.03) increased mean (37 ± 20 vs 60 ± 30 mmHg) and peak aortic valve pressure gradients (64 ± 37 vs 100 ± 53 mmHg) after 24 hr, with no significant difference (P = 0.99) in aortic valve area (0.6 ± 0.1 cm2). Baseline creatinine decreased from 159 ± 80 µmol·L–1 to 141 ± 80 µmol·L–1 after 24 hr (P = 0.04). One patient developed chest pain and one patient developed contrast nephropathy. There were no episodes of dyspnea, ischemic ECG changes, arrhythmias, or hypotension. All patients continued to receive nitroprusside until surgery, conversion to maintenance medical therapy, or death. Five patients died (two withdrawal of care, one multi-organ failure, one pulmonary embolism, one palliative comfort measures requested by family), 13 had aortic valve replacement, one had coronary artery bypass grafting (no aortic valve replacement as the annulus was too small), one balloon aortic valvuloplasty, and medical therapy in the remaining six patients. At 30 days, overall survival was 76%.
Conclusion: Nitroprusside in patients with severe aortic stenosis and reduced ejection fraction is a safe and effective bridge to more definitive surgical or medical treatment.
Funding: One investigator reported receiving funding for lecture fees.
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Commentary by N. M. Skjodt and D. R. Townsend |
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TOPArticle appraisedStructured abstractCommentary by N. M....References |
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The study by Khot et al. demonstrated improved hemodynamics and few side effects of nitroprusside in aortic stenosis patients with impaired cardiac function.3 This is contradictory to the traditional view of maintaining afterload in order to maintain coronary perfusion pressure.1
This study is small with only 25 patients. Although neither randomized, controlled, or blinded the physiologically-based objectives of this study beg clinical application. Each subject functioned as their own control. The patients were followed from the time of entry into study to completion of treatment and none were lost to follow-up. The echocardiographers and cardiac surgeons were blinded and concurred with the severity of aortic stenosis. There was only one exclusion criteria, hypotension. There were significant improvements in cardiac index, stroke volume and a decrease in systemic vascular resistance.
The authors’ findings suggest there are two components to afterload in patients with aortic stenosis. The fixed component is the mechanical valve stenosis, correctable only with surgery or valvuloplasty. The variable component during congestive heart failure may reflect the elevated adrenergic state that increases afterload and wall tension, worsening heart failure. This variable component is at least transiently reversible using nitroprusside to reduce afterload. In the absence of hypotension, these results can be applied to current management of severe aortic stenosis and reduced ventricular function as a bridge to further treatment including balloon valvuloplasty, valve replacement, or oral medical therapy.3
Those patients with hypertrophic cardiomyopathy and systolic motion of the anterior mitral valve would be at risk with this treatment.1,4 Dropping the afterload could reduce the gradient in the left ventricle outflow tract, decreasing cardiac output and worsening cardiac failure in this subset of aortic stenosis patients. A recent study suggests that transesophageal echocardiographic monitoring in the intensive care unit is associated with higher interobserver agreement in diagnosing and excluding significant causes of hemodynamic instability in postoperative cardiac patients.5 Would these patients be candidates for a transesophageal echocardiogram prior to proceeding with this treatment?
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References |
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TOPArticle appraisedStructured abstractCommentary by N. M....References |
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2 Aronow WS, Ahn C, Kronzon I, Nanna M. Prognosis of congestive heart failure in patients aged > or = 62 years with unoperated severe valvular aortic stenosis. Am J Cardiol 1993; 72: 846–8.[Medline]
3 Khot UN, Novaro GM, Popovic ZB, et al. Nitroprusside in critically ill patients with left ventricular dysfunction and aortic stenosis. N Engl J Med 2003; 348: 1756–63.
4 Konstadt S, Shernan S, and Oka Y. Clinical Transesophageal Echocardiography, 2nd ed. Lippincott-Williams and Wilkins; 2003: 97–100.
5 Costachescu T, Denault A, Guimond JG, et al. The hemodynamically unstable patient in the intensive care unit: hemodynamic vs. transesophageal echocardiographic monitoring. Crit Care Med 2002; 30: 1214–23.[Medline]
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