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Biomedical subjects

Marc A Silver

Publications and source records attributed to Marc A Silver.

At least 37 records · Page 2Linked to original sources
PubMed2003

Statin cardiomyopathy? A potential role for Co-Enzyme Q10 therapy for statin-induced changes in diastolic LV performance: description of a clinical protocol.

UNLABELLED: Lipid-lowering statins are thought to have a favorable safety profile. Statins inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the rate-limiting step of mevalonate synthesis. Mevalonate is the substrate for further synthesis of cholesterol and Co Enzyme Q10 (CoQ10). CoQ10 plays an important role during oxidative phosphorylation in the myocardial cell. Since myocardial diastolic function is a highly ATP dependent, we reasoned that early changes of diastolic function may be an early marker of ventricular dysfunction. METHODS: Patients who are to commence on statin therapy will be enrolled in the trial. Baseline measurements of plasma CoQ10, total cholesterol, LDL, HDL, CoQ10/LDL ratio, peak E, peak A velocities, E/A ratio, deceleration time, isovolumetric relaxation time, color M-mode propagation velocity will be performed and patients will then begin to take Oral atorvastatin (Lipitor, Parke-Davis) 20 mg daily for three to six months. All baseline measurement will be repeated after 3 to 6 months of statin therapy. Those patients demonstrating > 1 measurement of diastolic LV function that worsened during the 3 to 6 months of statin therapy will be supplemented with CoQ10 300 mg. daily for 3 months. A followup echocardiogram and blood CoQ10 level will be measured in patients who received CoQ10 supplementation. RESULTS: Statistical analysis will be performed using the paired t test to compare coenzyme levels and echocardiographic indices at baseline and after treatment and after supplementation.

Atorvastatin↗
PubMed2002

Short-term intravenous milrinone for acute exacerbation of chronic heart failure: a randomized controlled trial.

CONTEXT: Little randomized evidence is available to guide the in-hospital management of patients with an acute exacerbation of chronic heart failure. Although intravenous inotropic therapy usually produces beneficial hemodynamic effects and is labeled for use in the care of such patients, the effect of such therapy on intermediate-term clinical outcomes is uncertain. OBJECTIVE: To prospectively test whether a strategy that includes short-term use of milrinone in addition to standard therapy can improve clinical outcomes of patients hospitalized with an exacerbation of chronic heart failure. DESIGN: Prospective, randomized, double-blind, placebo-controlled trial conducted from July 1997 through November 1999. SETTING: Seventy-eight community and tertiary care hospitals in the United States. PARTICIPANTS: A total of 951 patients admitted with an exacerbation of systolic heart failure not requiring intravenous inotropic support (mean age, 65 years; 92% with baseline New York Heart Association class III or IV; mean left ventricular ejection fraction, 23%). INTERVENTION: Patients were randomly assigned to receive a 48-hour infusion of either milrinone, 0.5 microg/kg per minute initially (n = 477), or saline placebo (n = 472). MAIN OUTCOME MEASURE: Cumulative days of hospitalization for cardiovascular cause within 60 days following randomization. RESULTS: The median number of days hospitalized for cardiovascular causes within 60 days after randomization did not differ significantly between patients given milrinone (6 days) compared with placebo (7 days; P =.71). Sustained hypotension requiring intervention (10.7% vs 3.2%; P<.001) and new atrial arrhythmias (4.6% vs 1.5%; P =.004) occurred more frequently in patients who received milrinone. The milrinone and placebo groups did not differ significantly in in-hospital mortality (3.8% vs 2.3%; P =.19), 60-day mortality (10.3% vs 8.9%; P =.41), or the composite incidence of death or readmission (35.0% vs 35.3%; P =.92) CONCLUSION: These results do not support the routine use of intravenous milrinone as an adjunct to standard therapy in the treatment of patients hospitalized for an exacerbation of chronic heart failure.

Acute Disease↗
PubMed2002

Effect of nesiritide versus dobutamine on short-term outcomes in the treatment of patients with acutely decompensated heart failure.

OBJECTIVES: This study was designed to determine whether nesiritide, administered for acute decompensated congestive heart failure (CHF), affects healthcare costs by hospital length of stay (LOS), readmissions and short-term mortality, compared to dobutamine. BACKGROUND: Dobutamine is a commonly used inotropic treatment for CHF. Although dobutamine may have favorable hemodynamic and symptomatic effects, its use may be associated with side effects such as tachycardia, cardiac arrhythmias and myocardial ischemia. Nesiritide (B-type natriuretic peptide) is a new intravenous (IV) drug that produces hemodynamic and symptomatic improvement through balanced vasodilatory effects, neurohormonal suppression and enhanced natriuresis and diuresis. METHODS: From an open-label randomized study of nesiritide versus standard care (SC) in patients with CHF requiring hospitalization, we compared short-term outcome data from patients given nesiritide (0.015 or 0.03 microg/kg per min) with a subgroup of SC patients given dobutamine. A total of 261 patients are included in this analysis. RESULTS: Compared to dobutamine, both nesiritide doses were administered for a shorter total duration (p < 0.001), and the total duration of all IV vasoactive therapy (including study drug) was also shorter (p less-than-or-equal 0.012). Although there was no difference in LOS, there was a trend toward decreased readmissions in the two nesiritide groups (8% and 11%, respectively, vs. 20% in the dobutamine group). Six-month mortality was lower in the nesiritide groups. CONCLUSIONS: Treatment of decompensated CHF with nesiritide may lead to lower healthcare costs and reduced mortality compared to treatment with dobutamine.

Acute Disease↗
PubMedDate not supplied

Current and potential applications of left ventricular assist devices.

The syndrome of heart failure is epidemic, causing increased hospital admissions, poor survival rates, and a dismal quality of life. Treatment choices include pharmacologic, psychological, and surgical interventions. Recent data suggest that mechanical heart pumps, or assist devices, are viable additions or alternatives to transplantation in management of advanced heart failure. A ventricular assist device (VAD) can support the circulation when the natural heart is unable to maintain adequate perfusion. Although its use continues to be explored, VADs can be used in three ways: as a bridge to transplantation, as a destination therapy (or implanted permanently), or as a bridge to recovery. As VAD science advances, nurses will needs to understand its practice implications.

Cardiac Output, Low↗
PubMedDate not supplied

Left ventricular assist device weaning: hemodynamic response and relationship to stroke volume and rate reduction protocols.

Clinical evidence of myocardial recovery in a small cohort of patients supported with a left ventricular assist device (LVAD) has been reported. Development of an optimal LVAD weaning protocol is needed for these patients to sustain recovery after device explant. In this study, we tested the hypothesis that LVAD stroke volume reduction produces a steady-state mechanical reloading of left ventricular (LV) pressures and volumes compared with LVAD rate reduction that results in transient mechanical reloading of the heart due to beat-to-beat variation in LV pressures and volumes. The relationship of LVAD flow to LVAD stroke volume and systolic interval over a range of LVAD rates (60, 80, 100, 120, and 140 bpm) was validated in a mock circulatory flow loop. In six acute experiments, calves were implanted with a pneumatic paracorporeal LVAD (PVAD, Thoratec, Pleasanton, CA). The PVAD was operated asynchronously in the auto volume mode (full decompression) for 30 minutes to establish a baseline control condition. The calf hearts were then mechanically reloaded by LVAD rate reduction (80, 60, and 40 bpm) or LVAD stroke volume reduction (100, 120, and 140 bpm) protocols consisting of 30 minutes of support at each LVAD beat rate. The order of weaning protocols was randomized with a 30-minute recovery period (LVAD volume mode to fully decompress heart allowing it to rest) between protocols to enable return to baseline control state. Aortic pressure and flow, LV pressure and volume, pulmonary artery flow, and LVAD flow waveforms were recorded for each test condition. The LVAD stroke volume reduction protocol produced steady-state mechanical reloading compared with VAD rate reduction that resulted in transient LV mechanical reloading. This distinction is due to differences in their temporal relationships between LVAD and LV filling and emptying cycles. The acute hemodynamic benefit of LVAD stroke volume reduction was greater reduction in LV end-diastolic pressure and increase in LV segmental shortening than LVAD rate reduction. The long-term effects of steady-state and transient LV mechanical reloading on myocardial structure and function toward achieving sustained myocardial recovery warrant further investigation.

Animals↗
PubMedDate not supplied

High incidence of elevated B-type natriuretic peptide levels and risk factors for heart failure in an unselected at-risk population (stage A): implications for heart failure screening programs.

Only early detection and treatment is likely to stem the current epidemic of heart failure (HF). Several common cardiovascular and metabolic conditions increase the risk of developing symptomatic HF, but its detection by a simple and reliable screening method has proved elusive. HF screening sessions were conducted in September and November 2001. Members of the community with HF risk factors (e.g., hypertension, coronary artery disease, diabetes mellitus, hyperlipidemia) were invited--all specifically without a history of HF. The screening included a history review, health history questionnaire, measurement of blood pressure and pulse, as well as a measurement of B-type natriuretic peptide (BNP) level. A total of 233 individuals attended these two sessions: 108 men and 125 women (mean age, 63 years). Of the 233 subjects screened, the majority (92%) had >or=1 risk factor with an average of 2.8 risk factors for HF. The most common risks included hyperlipidemia (112), hypertension (112), age >65 years (105), cigarette smoking (105), coronary artery disease (60), and diabetes mellitus (54). Many subjects also had symptoms consistent with HF, with most (182, 82%) recording >or=1 symptom. Blood pressure measurements revealed a mean systolic of 139 mm Hg and mean diastolic of 79 mm Hg; on the screening days, 48% and 59% of subjects demonstrated either systolic or diastolic blood pressures above normal, respectively. BNP levels ranged from 0-479 pg/mL with an average of 40 pg/mL. A total of 24 subjects (10.3%) had a BNP level >100 pg/mL, and a total of 32 subjects (13.7%) had a level >80 pg/mL. The follow-up data showed that all 24 subjects saw their physician within 6 months after the screening. By 12 months following the initial screening program, 21 of the 24 subjects with elevated BNP levels (88%) underwent further testing and 18 of the 24 (67%) had changes in their medications. BNP screening identifies subjects at high risk for developing HF. Most subjects at risk have multiple risk factors and abnormal blood pressure. Approximately 10% of this population tested with an abnormal level of BNP, higher than the Food and Drug Administration-assigned cut-point diagnostic for HF. Increased public and physician awareness and information are needed to transform screening opportunities into a strategic approach to improve health care and HF prevention.

Female↗
PubMedDate not supplied

BNP Consensus Panel 2004: A clinical approach for the diagnostic, prognostic, screening, treatment monitoring, and therapeutic roles of natriuretic peptides in cardiovascular diseases.

Among the most exciting developments in the field of heart failure in recent times has been the rediscovery of the natriuretic peptide system and its pleuripotent effects on cardiac structure and function. This is particularly true of its natriuretic and hemodynamic effects. There has been an explosion of the knowledge base seeking to understand the wide range of homeostatic, regulatory, and counter-regulatory functions in which the natriuretic peptide system participates. Additional interest has been stimulated by advances in technology such as point-of-care and core laboratory BNP assays and the use of the recombinant B-type natriuretic peptide nesiritide as a treatment option. Despite this recent interest, the available literature lacks a comprehensive expert review of the current science and roles of natriuretic peptides for diagnostic, prognostic, screening, treatment monitoring, and therapeutic purposes. More importantly, a summary updating and guiding the clinician on most of these advances was lacking. An expert Consensus Panel with basic, methodological, and clinical expertise was convened to summarize current knowledge in these areas and the findings and consensus statements are contained herein.

Atrial Natriuretic Factor↗