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Teresa De Marco

Publications and source records attributed to Teresa De Marco.

18 recordsLinked to original sources
PubMed2006

Predictors of sudden cardiac death and appropriate shock in the Comparison of Medical Therapy, Pacing, and Defibrillation in Heart Failure (COMPANION) Trial.

BACKGROUND: The factors that determine the risk for sudden death or implantable cardioverter defibrillator therapy in patients receiving cardiac resynchronization therapy (CRT) therapies are largely unknown. METHODS AND RESULTS: We hypothesized that clinical measures of heart failure severity and the presence of comorbid conditions would predict the risk of malignant arrhythmias in the 1520 patients enrolled in the Comparison of Medical Therapy, Pacing, and Defibrillation in Heart Failure (COMPANION) Trial. Outcomes in the CRT group after implantable cardioverter defibrillator therapy were also evaluated. The CRT-defibrillator device reduced the risk of sudden death by 56% compared with drug therapy (17 of 595 [2.9%] versus 18 of 308 [5.8%], P<0.02). CRT therapy was not associated with sudden death risk reduction (48 of 617 [7.8%]). Other factors associated with reduced sudden death risk were left ventricular ejection fraction >20% (HR, 0.55 [95% CI, 0.35 to 0.87]; P=0.01), QRS duration >160 ms (HR, 0.63 [95% CI, 0.40 to 0.997]; P=0.05), and female gender (HR, 0.56 [95% CI, 0.34 to 0.94]; P=0.003). The risk for sudden death was increased by advanced New York Heart Association class IV heart failure (HR, 2.62 [95% CI, 1.61 to 4.26]; P<0.011) and renal dysfunction (HR, 1.69 [95% CI, 1.06 to 2.69]; P=0.03). An appropriate shock was experienced in 88 (15%) of the 595 CTR-D patients. In the CRT-defibrillator patients, female gender (HR, 0.54 [95 % CI, 0.31 to 0.94]; P=0.03) and use of neurohormonal antagonists were associated with reduced risk. Class IV heart failure status increased risk. Appropriate implantable cardioverter defibrillator therapy was positively associated with risk of death or all-cause hospitalization (HR, 1.57; P<0.002), pump failure death or hospitalization (HR, 2.35; P<0.001), and sudden death (HR, 2.99; P=0.03), but not total mortality (HR, 1.3; P=0.28). CONCLUSIONS: In CRT candidates, sudden cardiac death risk is associated with higher New York Heart Association class and renal dysfunction. In CRT-defibrillator recipients, reduction in the risk of an appropriate shock is associated with medical therapy with neurohormonal antagonists, female gender, and New York Heart Association functional class III versus IV clinical status. Shock therapy was associated with worse outcome.

Aged↗
PubMed2006

Nesiritide acutely increases pulmonary and systemic levels of nitric oxide in patients with pulmonary hypertension.

BACKGROUND: Pulmonary hypertension (PH) is characterized by decreased pulmonary vascular expression of nitric oxide (NOx), a vasodilator that increases levels of smooth muscle cyclic guanosine monophosphate (cGMP). This study investigated mechanisms by which the vasodilator B-type natriuretic peptide (BNP) affects the systemic and pulmonary vasculature in PH patients. METHODS AND RESULTS: Twenty PH patients with mean pulmonary artery (PA) pressure > 25 mm Hg were enrolled. Ten had precapillary (pulmonary capillary wedge pressure [PCWP] < or = 15 mm Hg) and 10 had postcapillary (PCWP > 15 mm Hg) PH. Right heart catheterization was performed before and 30 minutes after intravenous nesiritide infusion. NOx and cGMP levels from the PA and systemic (AO) arteries were obtained before and after nesiritide infusion. The postcapillary PH patients demonstrated significantly reduced pulmonary vascular resistance after nesiritide; there was no change in the precapillary PH cohort. NOx levels increased significantly in both AO (P < .0001) and PA (P = .0093), as did cGMP levels (P < .0001). There was a higher increase in NOx levels from the pulmonary arteries in precapillary PH patients compared to postcapillary PH patients (P = .020). CONCLUSION: In PH patients, nesiritide infusion significantly increases NOx levels, suggesting a novel mechanism for its vasodilatory effects. These responses may differ between pre- and postcapillary PH patients.

Adult↗
PubMed2005

Septal to posterior wall motion delay fails to predict reverse remodeling or clinical improvement in patients undergoing cardiac resynchronization therapy.

OBJECTIVES: The aim of this study was to test the hypothesis that a longer septal-to-posterior wall motion delay (SPWMD) would predict greater reverse remodeling and an improved clinical response in heart failure patients randomized to cardiac resynchronization therapy (CRT) in the CONTAK-CD trial. BACKGROUND: The SPWMD predicted clinical benefit with CRT in two previous studies from the same center. METHODS: In this retrospective analysis of the CONTAK-CD trial, SPWMD was measured from the baseline echocardiogram of 79 heart failure patients (ejection fraction 22 +/- 7%, QRS duration 159 +/- 27 ms, 72% ischemic, 84% male) randomized to CRT and compared with six-month changes in echocardiographic and clinical parameters. Patients with a left ventricular end-systolic volume index (LVESVI) reduction of at least 15% were considered responders. RESULTS: The feasibility and reproducibility of performing the SPWMD measurements were poor. Larger values for SPWMD did not correlate with six-month changes in left ventricular end-diastolic volume index (p = 0.26), LVESVI (p = 0.41), or left ventricular ejection fraction (p = 0.36). Responders did not have a significantly different SPWMD than non-responders (p = 0.26). The SPWMD did not correlate with measures of clinical improvement. At a threshold of SPWMD >130 ms, the test characteristics to predict reverse remodeling or a clinical response were inadequate. CONCLUSIONS: The previous findings that SPWMD predicts reverse remodeling or clinical improvement with CRT were not reproducible in patients randomized in the CONTAK-CD trial.

Aged↗
PubMed2005

Cost effectiveness of cardiac resynchronization therapy in the Comparison of Medical Therapy, Pacing, and Defibrillation in Heart Failure (COMPANION) trial.

OBJECTIVES: The analysis goal was to estimate incremental cost-effectiveness ratios (ICERs) for the Comparison of Medical Therapy, Pacing, and Defibrillation in Heart Failure (COMPANION) trial patients who received cardiac resynchronization therapy (CRT) via pacemaker (CRT-P) or pacemaker-defibrillator (CRT-D) in combination with optimal pharmacological therapy (OPT) relative to patients with OPT alone. BACKGROUND: In the COMPANION trial, CRT-P and CRT-D reduced the combined risk of all-cause mortality or first hospitalization among patients with advanced heart failure and intraventricular conduction delays, but the cost effectiveness of the therapy remains unknown. METHODS: In this analysis, intent-to-treat trial data were modeled to estimate the cost effectiveness of CRT-D and CRT-P relative to OPT over a base-case seven-year treatment episode. Exponential survival curves were derived from trial data and adjusted by quality-of-life trial results to yield quality-adjusted life-years (QALYs). For the first two years, follow-up hospitalizations were based on trial data. The model assumed equalized hospitalization rates beyond two years. Initial implantation and follow-up hospitalization costs were estimated using Medicare data. RESULTS: Over two years, follow-up hospitalization costs were reduced by 29% for CRT-D and 37% for CRT-P. Extending the cost-effectiveness analysis to a seven-year base-case time period, the ICER for CRT-P was 19,600 dollars per QALY and the ICER for CRT-D was 43,000 dollars per QALY relative to OPT. CONCLUSIONS: For the COMPANION trial patients, the use of CRT-P and CRT-D was associated with a cost-effectiveness ratio below generally accepted benchmarks for therapeutic interventions of 50,000 dollars per QALY to 100,000 dollars per QALY. This suggests that the clinical benefits of CRT-P and CRT-D can be achieved at a reasonable cost.

Cardiac Output, Low↗
PubMed2005

Clinical presentation, management, and in-hospital outcomes of patients admitted with acute decompensated heart failure with preserved systolic function: a report from the Acute Decompensated Heart Failure National Registry (ADHERE) Database.

UNLABELLED: Approximately 50% of patients hospitalized for heart failure have preserved systolic function. These patients are more likely to be older, women, and hypertensive. Their duration of hospitalization is similar to that of heart failure patients with systolic dysfunction, but their in-hospital mortality risk is lower. This mortality risk is increased in the setting of renal insufficiency, and the two most important risk predictors are elevated blood urea nitrogen and systolic blood pressure < or = 125 mm Hg. Medical treatment strategies for patients with preserved systolic function are inconsistent and reflect the need for efficacious evidence-based treatment regimens. OBJECTIVES: The aims of this analysis were to describe the clinical characteristics, management, and outcomes of patients hospitalized for acute decompensated heart failure (HF) with preserved systolic function (PSF). BACKGROUND: Clinically meaningful characteristics of these patients have not been fully studied in a large database. METHODS: Data from >100,000 hospitalizations from the Acute Decompensated Heart Failure National Registry (ADHERE) database were analyzed. RESULTS: Heart failure with PSF was present in 50.4% of patients with in-hospital assessment of left ventricular function. When compared with patients with systolic dysfunction, patients with PSF were more likely to be older, women, and hypertensive and less likely to have had a prior myocardial infarction or be receiving an angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker. In-hospital mortality was lower in patients with PSF compared with patients with systolic dysfunction (2.8% vs. 3.9%; adjusted odds ratio [OR]: 0.86; p = 0.005), but duration of intensive care unit stay and total hospital length of stay were similar. Serum creatinine >2 mg/dl was associated with increased in-hospital mortality in both systolic function groups (PSF: 4.8%; systolic dysfunction: 8.4%; p < 0.0001), and the most powerful predictors of in-hospital mortality in both groups were blood urea nitrogen >37 mg/dl (OR: 2.53; 95% confidence interval [CI]: 2.22 to 2.87) and systolic blood pressure < or =125 mm Hg (OR: 2.58; 95% CI: 2.33 to 2.86). CONCLUSIONS: Heart failure with PSF is common and is characterized by a unique patient profile. Event rates are worrisome and reflect a need for more effective management strategies.

Aged↗
PubMed2005

Effects of intravenous nesiritide on pulmonary vascular hemodynamics in pulmonary hypertension.

BACKGROUND: Nesiritide is effective in the treatment of decompensated heart failure (HF). We evaluated the acute hemodynamic effects of nesiritide, a recombinant B-type natriuretic peptide, in patients with HF and pulmonary hypertension (PH). METHODS AND RESULTS: Twenty patients with HF and PH (mean pulmonary arterial [PA] pressure >25 mm Hg) were enrolled: 10 with postpulmonary capillary wedge (PCW) >15 mm Hg and 10 with precapillary PH (PCW) < or =15. The pulmonary and systemic hemodynamics were determined by right heart catheterization at baseline and at 15 and 30 minutes after an intravenous nesiritide infusion (2 mcg/kg bolus and 0.01 mcg.kg.min). For the patients with postcapillary PH, the mean left ventricular ejection fraction was 28 +/- 15%. After the 30-minute nesiritide infusion, right atrial (RA) pressure decreased 48% (P < .0001), mean PA pressure decreased 29% (P < .0001), PCW pressure decreased 40% (P < .0001), cardiac index (CI) increased 35% (P = .009), pulmonary vascular resistance index (PVRI) decreased 35% (P = .01), and arteriovenous oxygen difference (AVDO(2)) decreased 27% (P = .0003). For precapillary PH patients, there was no change in RA, PA, or PCW pressure, nor any change in CI, PVRI, or AVDO(2). CONCLUSIONS: Nesiritide acutely and significantly reduced PA pressure, PVRI, and biventricular filling pressures in patients with postcapillary PH. However, for patients with precapillary PH, nesiritide had no significant acute hemodynamic effect on the pulmonary hemodynamics. The lack of acute beneficial effects of nesiritide in patients with advanced precapillary PH may be related to their relatively fixed remodeling of the pulmonary vasculature.

Adult↗
PubMed2005

Kaposi sarcoma-associated herpesvirus and primary and secondary pulmonary hypertension.

BACKGROUND: Kaposi sarcoma-associated herpesvirus (KSHV) has been implicated as a factor in the pathogenesis of primary pulmonary hypertension (PPH). We conducted a case-control study of patients with PPH and pulmonary hypertension (PH) associated with other disorders (secondary PH) to look for evidence of KSHV infection. MATERIALS AND METHODS: The study population was composed of patients with a diagnosis of PH at the University of California San Francisco Medical Center Department of Cardiology between July and November 2003. Serologic testing for KSHV was performed using enzyme-linked immunosorbent assays based on peptides from open reading frame-65 and K8.1, using sera from 19 patients with PPH, 29 patients with secondary PH, and 150 control subjects RESULTS: The overall seroprevalence of KSHV among all study participants was 2.0%. The rate among control subjects was 0.7% (1 of 150 subjects); among the study participants with PPH, we found no evidence of KSHV infection (0 of 19 patients). There was no significant difference between the observed seroprevalence of KSHV among patients with PPH compared to control subjects (p = 0.89). Of the 29 patients with a diagnosis of secondary PH, 3 patients (10.3%) were KSHV seropositive. Significantly, two of the three KSHV-infected secondary PH patients were also HIV positive, a known independent risk factor for KSHV infection and secondary PH. CONCLUSION: Our data do not support KSHV infection having a significant role in PPH or non-HIV-associated secondary PH compared to age- and gender-matched control subjects.

Antibodies, Viral↗
PubMed2004

Cardiac-resynchronization therapy with or without an implantable defibrillator in advanced chronic heart failure.

BACKGROUND: We tested the hypothesis that prophylactic cardiac-resynchronization therapy in the form of biventricular stimulation with a pacemaker with or without a defibrillator would reduce the risk of death and hospitalization among patients with advanced chronic heart failure and intraventricular conduction delays. METHODS: A total of 1520 patients who had advanced heart failure (New York Heart Association class III or IV) due to ischemic or nonischemic cardiomyopathies and a QRS interval of at least 120 msec were randomly assigned in a 1:2:2 ratio to receive optimal pharmacologic therapy (diuretics, angiotensin-converting-enzyme inhibitors, beta-blockers, and spironolactone) alone or in combination with cardiac-resynchronization therapy with either a pacemaker or a pacemaker-defibrillator. The primary composite end point was the time to death from or hospitalization for any cause. RESULTS: As compared with optimal pharmacologic therapy alone, cardiac-resynchronization therapy with a pacemaker decreased the risk of the primary end point (hazard ratio, 0.81; P=0.014), as did cardiac-resynchronization therapy with a pacemaker-defibrillator (hazard ratio, 0.80; P=0.01). The risk of the combined end point of death from or hospitalization for heart failure was reduced by 34 percent in the pacemaker group (P<0.002) and by 40 percent in the pacemaker-defibrillator group (P<0.001 for the comparison with the pharmacologic-therapy group). A pacemaker reduced the risk of the secondary end point of death from any cause by 24 percent (P=0.059), and a pacemaker-defibrillator reduced the risk by 36 percent (P=0.003). CONCLUSIONS: In patients with advanced heart failure and a prolonged QRS interval, cardiac-resynchronization therapy decreases the combined risk of death from any cause or first hospitalization and, when combined with an implantable defibrillator, significantly reduces mortality.

Adrenergic beta-Antagonists↗
PubMed2004

Effects of resynchronization therapy on cardiac function in pacemaker patients "upgraded" to biventricular devices.

INTRODUCTION: Cardiac resynchronization therapy (CRT) improves echocardiographic measures of cardiac function and has a variable effect on QRS duration in patients with left bundle branch block (LBBB). How CRT affects these indices in patients with right ventricular (RV) pacing-induced LBBB who are "upgraded" with left ventricular (LV) leads for CRT is unknown. We studied the echocardiographic effects of RV pacing and CRT in patients with prior continuous RV pacing after LV lead placement. METHODS AND RESULTS: Fifteen consecutive patients (age 73 +/- 11 years, LV ejection fraction 24 +/- 6%, QRS duration 190 +/- 27 msec) with New York Heart Association class IIIB-IV symptoms and continuous RV pacing underwent LV lead placement for CRT. Echocardiography and ECG were performed sequentially during RV pacing and CRT. CRT was associated with significantly reduced QRS duration (190 +/- 27 msec vs 165 +/- 18 msec, P = 0.005) and reduced LV electromechanical delay (180 +/- 33 msec vs 161+/- 43 msec). Baseline QRS duration correlated with CRT response. After CRT, patients had significant improvements in indices of systolic function, including LV ejection fraction, myocardial performance index (MPI), and LV ejection time. Abnormal baseline MPI was associated with greater improvement after CRT. LV end-diastolic and systolic volumes were similarly decreased with CRT. Mitral valve deceleration time, an index of diastolic function, was not affected by CRT. CONCLUSION: "Upgrading" RV paced patients with advanced heart failure to CRT improves measures of electrical and LV mechanical synchrony and improves systolic function.

Aged↗
PubMed2003

Cardiac resynchronization therapy for the treatment of heart failure in patients with intraventricular conduction delay and malignant ventricular tachyarrhythmias.

OBJECTIVES: This study was conducted to assess the safety and effectiveness of cardiac resynchronization therapy (CRT) when combined with an implantable cardioverter defibrillator (ICD). BACKGROUND: Long-term outcome of CRT was measured in patients with symptomatic heart failure (HF), intraventricular conduction delay, and malignant ventricular tachyarrhythmias (ventricular tachycardia/ventricular fibrillation [VT/VF]) requiring therapy from an ICD. METHODS: Patients (n = 490) were implanted with a device capable of providing both CRT and ICD therapy and randomized to CRT (n = 245) or control (no CRT, n = 245) for up to six months. The primary end point was progression of HF, defined as all-cause mortality, hospitalization for HF, and VT/VF requiring device intervention. Secondary end points included peak oxygen consumption (VO(2)), 6-min walk (6 MW), New York Heart Association (NYHA) class, quality of life (QOL), and echocardiographic analysis. RESULTS: A 15% reduction in HF progression was observed, but this was statistically insignificant (p = 0.35). The CRT, however, significantly improved peak VO(2) (0.8 ml/kg/min vs. 0.0 ml/kg/min, p = 0.030) and 6 MW (35 m vs. 15 m, p = 0.043). Changes in NYHA class (p = 0.10) and QOL (p = 0.40) were not statistically significant. The CRT demonstrated significant reductions in ventricular dimensions (left ventricular internal diameter in diastole = -3.4 mm vs. -0.3 mm, p < 0.001 and left ventricular internal diameter in systole = -4.0 mm vs. -0.7 mm, p < 0.001) and improvement in left ventricular ejection fraction (5.1% vs. 2.8%, p = 0.020). A subgroup of patients with advanced HF (NYHA class III/IV) consistently demonstrated improvement across all functional status end points. CONCLUSIONS: The CRT improved functional status in patients indicated for an ICD who also have symptomatic HF and intraventricular conduction delay.

Aged↗
PubMed2003

Role of nonglycosidic inotropic agents: indications, ethics, and limitations.

Nonglycosidic inotropic agents have been used for the short-term management of low output states and hypotension complicating acute myocardial infarction for several years. Without adequate reperfusion of the ischemic myocardium, inotropic agents are seldom effective in producing sustained hemodynamic responses. Furthermore, the potential exists for enhancement of ischemia and extension of myocardial necrosis. Thus, inotropic and vasopressors therapy should be regarded as temporary supportive treatment in patients with acute coronary syndrome and should be discontinued as soon as feasible. Parenteral sympathomimetic agents, usually dobutamine, and phosphodiesterase inhibitors, usually milrinone, are used for the management of exacerbations of chronic systolic heart failure. Although hemodynamics, and occasionally clinical status, improve, such therapy is associated with increased mortality and can potentially hasten a patient's demise. Nonparenteral sympathomimetics, such as ibopamine, phosphodiesterase-III inhibitors, such as milrinone and enoximone, calcium-sensitizing agents, such as pimobendan, and other novel inotropic agents, such as vesnarinone, all increase mortality of patients with chronic heart failure. Furthermore, newer noninotropic agents, such as B-natriuretic peptide, have been introduced for treatment of decompensated heart failure. New nonpharmacologic devices, such as biventricular pacing, are available for the treatment of advanced heart failure. Thus, indications for the use of presently available nonglycosidic inotropic agents are limited and should be considered only for short-term therapy or when no other treatment is available.

Adrenergic beta-Antagonists↗
PubMed2003

Isolated bundle branch block and left ventricular dysfunction.

BACKGROUND: Population studies have identified the presence of bundle branch block (BBB) as a risk factor for increased mortality in patients with known cardiac disease. It is unknown how chronic ventricular dyssynchrony resulting solely from conduction delay affects ventricular function. METHODS AND RESULTS: Subjects were retrospectively identified from the University of California, San Francisco, electrocardiogram database with QRS prolongation. Subjects who had no evidence of heart disease and had baseline and serial studies evaluating ongoing risk of coronary artery disease status and left ventricular function were followed over time. Documentation of a minimum of 2 serial evaluations of cardiac status were present in a total of 51/176 (20%) subjects with isolated BBB who constitute the study population. After a mean follow-up of 52 +/- 45 months-adjusting for differences due to age, sex, the presence of hypertension, hyperlipidemia, and diabetes mellitus-left ventricular ejection fraction diminished by -7.3 +/- 12% per year in the isolated left BBB cohort versus -1.9 +/- 4% in isolated right BBB cohort and -1.1 +/- 3% reduction in the isolated nonspecific intraventricular conduction delay cohort (P =.019). CONCLUSIONS: Left bundle branch block itself may be a cause of ventricular dysfunction.

Aged↗
PubMed2002

Pulmonary hypertension: hemodynamic diagnosis and management.

Hemodynamic classification of pulmonary hypertension relates to the hemodynamic mechanisms of pulmonary arterial hypertension, such as abnormalities of pulmonary blood flow, pulmonary vascular resistance, and pulmonary venous pressures. The therapeutic approaches can be directed to the hemodynamic mechanisms of pulmonary hypertension.

Hemodynamics↗
PubMed2002

Effects of long-term biventricular stimulation for resynchronization on echocardiographic measures of remodeling.

BACKGROUND: Long-term ventricular resynchronization therapy improves symptom status. Changes in left ventricular remodeling have not been adequately evaluated. METHODS AND RESULTS: Fifty-three patients with systolic heart failure and bundle-branch block underwent implantation of biventricular stimulation (BVS) devices as part of a randomized trial. Echocardiograms were acquired at randomization and at 6-week intervals until completion of 12 weeks of continuous BVS. There were no changes in heart rate or QRS duration after 12 weeks of BVS. Serum norepinephrine values did not change with BVS. After 12 weeks of BVS, left atrial volume decreased. Left ventricular end-systolic and end-diastolic dimensions and left ventricular end-systolic volume also decreased after 12 weeks of BVS. Sphericity index did not change. Measures of systolic function, including left ventricular outflow tract and aortic velocity time integral and myocardial performance index, improved. CONCLUSIONS: Long-term resynchronization therapy results in atrial and ventricular reverse remodeling and improved hemodynamics.

Adult↗
PubMedDate not supplied

Pulmonary arterial hypertension and women.

Pulmonary arterial hypertension (PAH) is a progressive disorder with a poor prognosis. It is characterized by sustained elevation of pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR). It is defined hemodynamically by a mean PAP over 25 mm Hg, a pulmonary arterial wedge pressure of 15 mm Hg or less (which excludes left sided lesions), and a PVR of 3 or more Wood units (240 dyn.sec.cm-5). Patients are limited by exertional dyspnea, pre- or true syncope, chest pain, and edema/ascites when right heart failure supervenes. PAH afflicts predominantly young women and the diagnosis is often delayed. Three processes contribute to progressive arterial narrowing: vasoconstriction, vascular remodeling, and thrombosis in situ. The diagnosis of PAH must be confirmed and its etiology must be identified before appropriate therapy can be instituted. Right heart catheterization is necessary to establish the diagnosis, severity, and prognosis of PAH and to ascertain its etiology and to evaluate vasoreactivity, which guides therapy. Treatment of PAH includes vasodilators, supplemental O2, anticoagulation, diuretics, digoxin, intravenous inotropic therapy for decompensated right ventricular failure, and lung or combined heart-lung transplantation for those patients who continue to deteriorate with a poor quality of life despite pharmacologic therapy. Calcium channel blockers are beneficial in a small minority of patients. Prospective, controlled, randomized trials of approved vasodilator agents have enrolled a large proportion of women (70-85%). Agents such as the endothelin-1 receptor antagonist bosentan, the phosphodiesterase-5 inhibitor sildenafil, and the prostanoids have been shown to improve symptoms, exercise capacity, and, in most instances, delay clinical worsening. The clinical outcomes of patients with PAH have improved with the judicious use of contemporary therapies.

Cardiac Catheterization↗