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Biomedical subjects

Roger M Mills

Publications and source records attributed to Roger M Mills.

12 recordsLinked to original sources
PubMed2004

Plasma B-type natriuretic peptide levels predict postoperative atrial fibrillation in patients undergoing cardiac surgery.

BACKGROUND: Postoperative (postop) atrial fibrillation (AF) occurs in up to 60% of patients after cardiac surgery, leading to longer hospital stays and increased healthcare costs. Recently, B-type natriuretic peptide (BNP) has been reported to predict occurrence of nonpostoperative AF. This study evaluates whether elevated preoperative (preop) plasma BNP levels predict the occurrence of postop AF. METHODS AND RESULTS: One hundred eighty-seven patients with no history of atrial arrhythmia who had a preoperative BNP level and had undergone cardiac surgery were identified. Their records were reviewed, and postoperative ECG and telemetry strips were analyzed for AF until the time of discharge. Postop AF was documented in 80 patients (42.8%). AF patients were older (68+/-11 versus 64+/-14 years, P=0.04), but there was no difference in sex distribution, hypertension, left ventricular (LV) function, LV hypertrophy (LVH), left atrial size, history of coronary artery disease (CAD), or beta-blocker use. Preop plasma BNP levels were higher in the postop AF patients (615 versus 444 pg/mL, P=0.005). After adjustment for age, sex, type of surgery, hypertension, LV function, LVH, left atrial size, CAD, and beta-blocker use, the odds ratios of postop AF according to increasing quartiles, compared with patients with lowest quartile, were 1.8, 2.5, and 3.7 (P(trend)=0.03). CONCLUSIONS: An elevated preop plasma BNP level is a strong and independent predictor of postop AF. This finding has important implications for identifying patients at higher risk of postop AF who could be considered for prophylactic antiarrhythmic or beta-blocker therapy.

Aged↗
PubMed2003

Comparison of effectiveness of carvedilol versus metoprolol or atenolol for atrial fibrillation appearing after coronary artery bypass grafting or cardiac valve operation.

A retrospective review of 115 patients who underwent cardiac surgery demonstrated a marked reduction in postoperative atrial fibrillation (8% vs 32%, p <0.05) in patients who received carvedilol versus metoprolol or atenolol immediately after surgery. A prospective study examining the possibility of carvedilol's greater efficacy in preventing postoperative atrial fibrillation appears warranted.

Adult↗
PubMed2003

Nitroprusside in critically ill patients with left ventricular dysfunction and aortic stenosis.

BACKGROUND: Vasodilators are considered to be contraindicated in patients with severe aortic stenosis because of concern that they may precipitate life-threatening hypotension. However, vasodilators such as nitroprusside may improve myocardial performance if peripheral vasoconstriction is contributing to afterload. METHODS: We determined the response to intravenous nitroprusside in 25 patients with severe aortic stenosis and left ventricular systolic dysfunction. Patients were included in the study if they had been admitted to the intensive care unit for invasive hemodynamic monitoring of heart failure and if they had a depressed ejection fraction (<or=0.35), severe aortic stenosis (aortic-valve area, <or=1 cm2), and a depressed cardiac index (<or=2.2 liters per minute per square meter). Patients were excluded if they had hypotension, defined as either the need for intravenous inotropic or pressor agents or a low mean systemic arterial pressure (<60 mm Hg). Patients were enrolled irrespective of other, coexisting valve disease or coronary artery disease. RESULTS: At base line, the mean (+/-SD) ejection fraction was 0.21+/-0.08; the aortic-valve area was 0.6+/-0.2 cm2, with peak and mean gradients of 65+/-37 and 39+/-23 mm Hg, respectively; and the cardiac index was 1.60+/-0.35 liters per minute per square meter. After six hours of therapy with nitroprusside (at which time the dose had been increased to a mean of 103+/-67 microg per minute), the cardiac index had increased to 2.22+/-0.44 liters per minute per square meter (P<0.001 for the comparison with base line). After 24 hours of nitroprusside infusion (dose, 128+/-96 microg per minute), the cardiac index had increased further, to 2.52+/-0.55 liters per minute per square meter (P<0.001 for the comparison with base line). Nitroprusside was well tolerated and had minimal side effects. CONCLUSIONS: Nitroprusside rapidly and markedly improves cardiac function in patients with decompensated heart failure due to severe left ventricular systolic dysfunction and severe aortic stenosis. It provides a safe and effective bridge to aortic-valve replacement or oral vasodilator therapy in these critically ill patients.

Aged↗
PubMed2003

High-dose angiotensin-converting enzyme inhibition restores body fluid homeostasis in heart-transplant recipients.

OBJECTIVES: We tested the hypothesis that salt and fluid retention in heart-transplant recipients (HTRs) is caused by a failure to reflexively suppress the renin-angiotensin-aldosterone system (RAAS). BACKGROUND: It is known that extracellular fluid volume is expanded (12% to 15%) in HTRs who develop hypertension. METHODS: Responses to volume expansion were measured in eight HTRs (ages 57 +/- 6 years) and six liver-transplant recipients (LTRs) (ages 52 +/- 2 years) both before and after treatment with captopril (225 mg/day). After three days of a standardized diet, 0.154 mol/l saline was infused at 8 ml/kg/h for 4 h. Blood pressure, hormones, and renal function were monitored for 48 h. After four months, the same subjects received captopril (225 mg/day), and the protocol was repeated. RESULTS: Before captopril, saline infusion suppressed the RAAS in LTRs but not in HTRs, resulting in elimination of 86 +/- 12% versus 50 +/- 11% of the sodium load by 48-h postinfusion. Blood pressure increased only in the HTRs (+16 +/- 5/9 +/- 3 mm Hg) and remained elevated for 48 h (p < or = 0.05). After captopril, sodium elimination was comparable in the liver (87 +/- 13%) and heart groups (86 +/- 12%) and blood pressure did not change in either group. CONCLUSIONS; Heart transplant recipients have blunted diuretic and natriuretic responses to volume expansion that is mediated by their inability to suppress the RAAS. Pharmacologic suppression of the RAAS normalized defects in blood pressure and fluid homeostasis. These findings indicate that hypertension in HTRs is caused, in part, by a failure to reflexively suppress the RAAS when these patients become hypervolemic.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2003

Does chronic ST segment elevation following Q wave myocardial infarction exclude tissue viability?

PURPOSE: Electrocardiographic (ECG) ST segment elevation lasting 2 or more weeks following Q wave myocardial infarction has been associated with 'ventricular aneurysm' and absence of tissue viability. Regional systolic dysfunction may reflect either viable myocardium or scar. Positron emission-tomographic (PET) imaging can distinguish viable from nonviable tissue. We hypothesized that patients with chronic ST segment elevation after Q wave infarction might demonstrate salvageable myocardium in the infarct region. METHODS: The ECGs of 1,229 sequential patients undergoing PET scans for viability assessment were reviewed by an electrocardiographer to identify individuals with chronic anteroseptal Q wave infarctions with persistent ST segment elevation exceeding 1 mV. Patients with QRS duration longer than 0.14 ms or rhythm other than sinus were excluded. Viability was considered present if either a reversible stress-induced perfusion defect (ischemia) or a resting perfusion-metabolism mismatch (hibernation) was identified. RESULTS: Anteroseptal ECG Q wave infarction was identified in 132 subjects (74% male, age 61 +/- 12 years). Chronic ST segment elevation was present in 84 subjects (64%) and absent in 48. Baseline clinical characteristics and left ventricular systolic function were similar in both groups. 63% of those with and 56% of those without chronic ST elevation had viable myocardium. No relationship was noted between chronic ST segment elevation and the presence or absence of myocardial viability. CONCLUSIONS: Chronic ST segment elevation after anteroseptal Q wave myocardial infarction does not exclude myocardial viability in the 'infarct zone'. Evaluation of residual tissue viability is indicated to assess the benefit of revascularization in patients with Q wave infarction and chronic ST segment elevation.

Aged↗
PubMed2003

Nesiritide in perspective: evolving approaches to the management of acute decompensated heart failure.

Nesiritide is currently indicated for the management of acute decompensated heart failure defined by the presence of volume overload and dyspnea at rest or with minimal activities. Hypotension and cardiogenic shock are the major contraindications to nesiritide use. The recommended dosing schedule is a 2 micro g/kg bolus followed by a 0.01 micro g/kg/min infusion. Some clinicians, however, opt to begin the infusion at the recommended dose without a loading bolus in nonemergency situations. The average duration of infusion in the Vasodilation in the Management of Acute Congestive Heart Failure (VMAC) trial was approximately 28 hours. Clinical efficacy endpoints included resolution of dyspnea and reduction of volume overload. Appropriate oral drug therapy for heart failure management should be initiated during the nesiritide infusion. The 15-year transition of B-type natriuretic peptide from a newly discovered physiologic entity to clinical use in the diagnosis and treatment of heart failure provides a remarkable example of rapid technological improvement and enhanced clinical understanding. As with most advances, the process of rolling back the frontiers of knowledge has posed even more questions. However, we must not overlook the progress to date, simply because all of the answers are not yet available.

Acute Disease↗
PubMed2002

How to use nesiritide in treating decompensated heart failure.

Nesiritide (Natrecor), a synthetic formulation of B-type natriuretic peptide (BNP), is the first new parenteral agent to be approved for treating heart failure in more than a decade. In patients hospitalized with decompensated congestive heart failure, nesiritide promptly reduces pulmonary capillary wedge pressure, pulmonary arterial pressure, right atrial pressure, and systemic vascular resistance, resulting in clinical improvement.

Atrial Natriuretic Factor↗
PubMedDate not supplied

"BNP" for heart failure: role of nesiritide in cardiovascular therapeutics.

B-type natriuretic peptide, or nesiritide, recently gained US Food and Drug Administration approval as the first new parenteral agent approved for heart failure therapy in more than a decade. Nesiritide refers to a peptide identical to endogenous B-type natriuretic peptide, currently manufactured by recombinant DNA technology. Nesiritide has been evaluated in clinical trials involving more than 700 subjects. The drug produces a prompt fall in systemic vascular resistance and pulmonary capillary wedge pressure, associated with rapid clinical improvement in decompensated heart failure. Nesiritide represents an attractive choice for first-line therapy of acutely decompensated heart failure patients. In this review, the authors summarize the currently available data regarding the use of nesiritide, and offer recommendations for its use based on our experience with the compound in clinical trials.

Atrial Natriuretic Factor↗