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Biomedical subjects

Theo E Meyer

Publications and source records attributed to Theo E Meyer.

At least 19 recordsLinked to original sources

Use of disease-modifying therapies in patients hospitalized with heart failure: a population-based perspective.

BACKGROUND: Little data are available about the hospital management of patients with decompensated heart failure (HF) with individual and combination medical therapies, particularly from the more generalizable perspective of a population-based investigation. The purpose of our study was to describe the use of different cardiac medications in 2463 patients with new-onset HF who were discharged from all greater Worcester, Massachusetts, hospitals during 2000. METHODS: On the basis of a review of medical records, we examined the prescribing of 2 classes of cardiac medications that have been shown to improve the long-term prognosis of patients with HF (angiotensin pathway inhibitors and beta-blockers). We also examined the use of 2 therapies commonly used to improve the symptomatic status of patients with acute HF (diuretics and digoxin). RESULTS: The mean age of the study sample was 76 years, and 57% were women. Approximately 1 in 5 patients were not prescribed beta-blockers or angiotensin inhibitors during their index hospitalization, whereas 1 in 3 patients were discharged with both of these effective cardiac medications. Diuretics were prescribed for virtually all patients (98%), followed by the use of digoxin in approximately half of patients (48%). The receipt of both beta-blockers and angiotensin pathway inhibitors was associated with several demographic, medical history, and clinical factors. Patients treated with both effective cardiac medications were also more likely to be counseled to monitor or modify several lifestyle factors that have been shown to be effective adjuncts to the medical management of patients with HF. CONCLUSIONS: Considerable opportunity remains for the more optimal hospital management of patients with decompensated HF.

Adrenergic beta-Antagonists↗

Adenosine A1 receptor expression during the transition from compensated pressure overload hypertrophy to heart failure.

OBJECTIVES: Myocardial adenosine is increased in pressure-overload hypertrophy (POH) and exerts important cardioprotective effects that delay transition to left ventricular failure. Adenosine-mediated signaling is attenuated in POH, but whether this depends on receptor or postreceptor defects is unknown. We therefore examined left ventricular adenosine A1-receptor gene and protein expression in experimental POH. METHODS: Six week-old Sprague-Dawley rats were subjected to abdominal aortic banding (group B) or sham operation (group S). Echocardiography and left ventricular catheterization were performed 10 weeks later under ketamine anesthesia. Left ventricular and lung weight indices were obtained postmortem. A1-Receptor mRNA and protein expression were measured in samples from left ventricular, right ventricular and aortic arch tissue. Group B rats were subgrouped as having compensated or decompensated hypertrophy according to the absence or presence of lung congestion (lung weight index below or above mean +/- 2SD compared with group S rats). RESULTS: Both mRNA and protein A1-receptor expression were significantly increased in compensated group B versus group S rats (by, respectively, 37 and 77%; both P < 0.01). This was not observed in decompensated group B rats. No consistent gene or receptor expression changes were observed in right ventricular or aortic tissues. CONCLUSIONS: In compensated POH, increased interstitial adenosine concentrations are accompanied by increased expression of the specific receptor mediating the major cardioprotective effects of this autacoid. Such overexpression is no longer detectable once the transition from POH to left ventricular failure has occurred. These observations may have pathophysiological and, in perspective, therapeutic relevance to the course of hypertensive heart disease.

Animals↗

Use of nonpharmacologic treatment approaches in patients with heart failure.

BACKGROUND: Patient education has been shown to beneficially impact the utilization of medical resources and certain outcomes in patients hospitalized with heart failure (HF). Little data are, however, available about the implementation of patient education and counseling of patients with HF in the community setting. The purpose of the present investigation was to examine the extent of health care provider recommendations for the monitoring or modification of lifestyle approaches or dietary factors in patients with new onset HF discharged from all greater Worcester (MA) hospitals in 2000. METHODS: The study sample consisted of 2411 metropolitan Worcester residents hospitalized at all 11 area medical centers with acute HF. Based on the review of medical records, we examined provider recommendations for the monitoring or modification of 5 lifestyle factors including salt restriction, dietary changes, increased physical activity, limitation of fluids, and daily monitoring of weight in hospital survivors of HF. RESULTS: Among all patients, approximately 22% were recommended to change either no or 1 lifestyle related factor, 2 in every 5 patients received recommendations to alter any 2 lifestyle characteristics, while 1 in 6 were counseled about the importance of monitoring or modifying 4 or more lifestyle or dietary factors. Physician counseling was associated with several demographic and clinical factors. Documentation of none or few patient education recommendations was also associated with the failure to receive multiple effective medical therapies for HF. CONCLUSIONS: The results of our community-wide investigation suggest that considerable opportunity remains for the more effective hospital counseling of patients with acute HF.

Age Distribution↗

Analysis of left ventricular systolic function using midwall mechanics in patients >60 years of age with hypertensive heart disease and heart failure.

Normal ejection fraction (EFs) is often equated with normal systolic function. However, midwall mechanics reveal systolic dysfunction in hypertensive heart disease accompanied by hypertrophic remodeling. Midwall mechanics are unstudied in patients with acute diastolic heart failure (HF). This study analyzed left ventricular (LV) midwall stress-shortening relations in 61 patients aged >60 years with hypertensive heart disease, HF, and normal EF. Sixty-one hypertensive patients (mean age 78 +/- 10 years) who presented with HF, each with an EF >50%, underwent echocardiography. Midwall mechanics were compared with those of 79 controls (mean age 75 +/- 8 years) without structural heart disease. Relative wall thickness (0.63 +/- 0.11 vs 0.46 +/- 0.10 mm) and LV mass (237 +/- 67 vs 177 +/- 57 g) were significantly greater in patients with HF compared with controls. Mean EFs were similar in patients with HF and controls (64 +/- 9% vs 67 +/- 9%). Although mean endocardial fractional shortening (35 +/- 7% vs 37 +/- 7%) was not significantly different, midwall shortening in patients with HF was significantly less compared with controls (16 +/- 2% vs 19 +/- 3%, p <0.05). Eighteen of the 61 patients with HF (30%) had midwall shortening that was <95% confidence intervals of the normal midwall stress-shortening relations. By this criterion, these patients had systolic dysfunction despite normal EF; they had smaller LV chambers (in dimension and volume), greater relative wall thickness, and smaller stroke volumes. In conclusion, almost 1/3 of patients hospitalized with diastolic HF had systolic dysfunction, characterized by abnormal midwall stress-shortening relations.

Aged↗

Incidence and hospital death rates associated with heart failure: a community-wide perspective.

PURPOSE: Despite often stated references to the emerging epidemic of heart failure in the United States, relatively little data are available describing the incidence and short-term death rates associated with this clinical syndrome. The objectives of this study were to describe the hospital incidence and death rates associated with acute heart failure and factors associated with an adverse hospital prognosis in residents of the Worcester, Mass, metropolitan area hospitalized at all greater Worcester medical centers with new onset heart failure in 2000. SUBJECTS AND METHODS: We reviewed the medical records of patients hospitalized for acute heart failure at all 11 area medical centers during 2000. New onset heart failure was diagnosed using standardized criteria. Regression analyses were performed to examine demographic and clinical factors associated with hospital death rates. RESULTS: During 2000, 2604 men and women from greater Worcester were diagnosed with new onset heart failure; 637 (24.5%) of these cases were initial events. The incidence and attack rates (per 100,000) of heart failure were 219 and 897, respectively. Occurrence of heart failure increased with advancing age, and women were at greater risk for heart failure than men (incidence rates [per 100,000] = 250 and 194, respectively). Hospital case-fatality rates were 5.1%. Hospital death rates were associated with several demographic and clinical characteristics. CONCLUSIONS: The results of this study suggest that heart failure is an important clinical syndrome affecting residents of this large northeast community. Several groups at high risk for developing or dying from heart failure can be identified and targeted for preventive efforts as well as for the receipt of effective treatment modalities.

Aged↗

Brain natriuretic peptide levels fall rapidly after cardioversion of atrial fibrillation to sinus rhythm.

BACKGROUND: Brain natriuretic peptide (BNP) levels have been reported to fall following cardioversion of atrial fibrillation (AF). The mechanism for the fall in BNP has not been elucidated and the potential confounding effects of sedation have not been investigated. Sedation may alter BNP levels via its effects on loading conditions. Accordingly, we studied whether BNP levels change shortly after cardioversion and attempted to control for possible effects of sedation. METHODS: BNP levels were obtained before and after cardioversion in patients with AF and in a control group of patients undergoing intravenous conscious sedation for transesophageal echocardiography. RESULTS: BNP levels dropped (260 +/- 255 vs. 190 +/- 212 pg/ml, p < 0.05) 40 min after cardioversion, decreasing in 33 of 41 subjects who achieved sinus rhythm. By contrast, mean BNP did not fall in subjects in whom cardioversion was not successful. The change in BNP level was not related to the degree of change in heart rate. No control subject experienced a change in cardiac rhythm; BNP levels increased (195 +/- 407 vs. 238 +/- 458 pg/ml, p < 0.05) in 18/22 subjects after sedation. Baseline BNP levels were elevated in subjects with AF, and BNP levels were elevated in parallel with heart failure symptoms. CONCLUSIONS: The rapid fall in BNP after cardioversion (1) may reflect prompt hemodynamic improvement associated with rhythm change and (2) does not appear to be due to the effects of sedation.

Adult↗

Paradoxical changes in brain natriuretic peptide levels and loading conditions after intravenous conscious sedation.

BACKGROUND: Elevated filling pressure and wall stress have been proposed as stimuli for elevated brain natriuretic peptide (BNP) levels. Narcotic and benzodiazepine sedation, such as is used for transesophageal echocardiography (TEE), is known to decrease filling pressures. We hypothesized that lower filling pressure and wall stress associated with intravenous conscious sedation (IVCS) would lead to lower BNP levels. METHODS: We studied BNP levels, blood pressure, and echocardiographic indices of filling pressure and wall stress before and after IVCS and TEE. RESULTS: When data before and after IVCS and TEE were compared, mean blood pressure decreased (149 +/- 24/83 +/- 14 mm Hg vs 126 +/- 29/69 +/- 14; P < .01), as did mitral Doppler E wave velocity (82 +/- 23 cm/s vs 76 +/- 22; P < .05), right ventricular/atrial gradient (31 +/- 10 mm Hg vs 29 +/- 13; P < .05), and wall stress. However, BNP levels increased (195 +/- 407 pg/mL vs 238 +/- 458; P < .01). CONCLUSIONS: In a series of patients undergoing clinically indicated TEE, BNP levels increase above baseline after IVCS. The increase in BNP occurs despite lower blood pressure, lower mitral Doppler E velocity, lower right ventricular/atrial gradient, and lower wall stress compared with baseline. The mechanism of the paradoxical increase in BNP is not entirely clear, but it may conceivably be a result of counterregulatory hormone release caused by acute decrease in blood pressure.

Adult↗

Receptors subtypes involved in adenosine-mediated modulation of norepinephrine release from cardiac nerve terminals.

The objective of this study was to determine which adenosine receptor subtypes were involved in the modulation of norepinephrine release from cardiac nerve terminals. In addition, the persistence of adenosine-mediated effects was evaluated. Rat hearts attached to the stellate ganglion were isolated and perfused. The ganglion was electrically stimulated twice (S1 and S2), allowing 10 min between the stimulations. To determine adenosine receptor subtypes, selective and nonselective adenosine agonists and antagonists were infused following S1 and until the end of S2. To evaluate the persistence of adenosine-mediated effect on norepinephrine release, the stellate ganglion was stimulated a third (S3) and fourth (S4) time. Coronary effluents were collected to determine norepinephrine content. Adenosine and a selective A1 receptor agonist, CCPA, inhibited norepinephrine release by 49% and 54%, respectively. This effect was reversed by simultaneous infusion of nonspecific (8-SPT) and specific (DPCPX) A1 receptor antagonists. Selective A2A (CGS 21680) and A3 (AB-MECA) receptor agonists had no discernible effect on norepinephrine release. Similarly, adenosine A2A receptor antagonists CSC and DMPX did not alter the dose-response relation between norepinephrine release and adenosine. Finally, the inhibitory effects of adenosine on norepinephrine release did not persist 10 min subsequent to the removal of adenosine. Adenosine inhibited norepinephrine release primarily via the adenosine A1 receptor. This effect of adenosine was of short duration. Adenosine A2A and A3 receptors were either absent or functionally insignificant in the regulation of norepinephrine release in the rat heart.

Adenosine↗

A syndrome of transient left ventricular apical wall motion abnormality in the absence of coronary disease: a perspective from the United States.

BACKGROUND: The syndrome of chest pain associated with characteristic anterior electrocardiographic changes, moderate increases in cardiac enzymes, and a reversible apical wall motion abnormality in the absence of coronary artery disease has been documented in Japan, but has received relatively little attention in other countries. METHODS: The clinical and echocardiographic data of 12 patients (11 women, mean age 64 +/-14 years) who presented with chest symptoms, electrocardiographic (ECG) changes indicative of an acute anteroapical myocardial infarction, abnormal cardiac enzyme levels and echocardiography showing an apical wall motion abnormality were collected. Coronary angiography was performed in 10 patients. A follow-up echocardiogram was obtained within 2 weeks of the initial diagnosis in most cases. RESULTS: An identifiable, precipitating ("trigger") event could be identified in all 12 individuals. Respiratory distress was present in 7, the death of a relative in 3, in 4 a surgical or medical procedure had been performed, and in 1 a panic disorder was diagnosed. The echocardiograms showed a characteristic wall motion pattern of significant apical dysfunction. All of the patients who underwent coronary arteriography had noncritical coronary artery disease. Follow-up echocardiography showed normalization of the LV dysfunction in all instances. CONCLUSION: We identified a syndrome of chest pain, dyspnea, ECG and enzyme changes mimicking acute myocardial infarction, similar to the "Takotsubo" syndrome described in Japan. It is likely that the widespread use of echocardiography, coupled with increased recognition of this syndrome, will result in this diagnosis being made more commonly.

Adrenergic beta-Antagonists↗

Heterogeneity in the management and outcomes of patients with acute myocardial infarction complicated by heart failure: the National Registry of Myocardial Infarction.

BACKGROUND: Heart failure (HF) is an important predictor of poor outcome after acute myocardial infarction (AMI). However, limited data exist about the clinical significance of HF in the coronary reperfusion era and the impact of its timing on hospital outcomes. The objective of this study was to determine the clinical impact of HF complicating AMI in the National Registry of Myocardial Infarction (NRMI). A secondary objective was to determine differences in demographic and clinical characteristics, treatment, and hospital death rates in patients presenting with HF compared with those developing HF after presentation. METHODS AND RESULTS: The study sample consisted of patients with AMI and without a history of HF included in the NRMI. Of 606 500 cases included from July 1, 1994 to June 30, 2000, 123 938 (20.4%) patients had HF at the time of hospital presentation and 52 220 (8.6%) developed HF thereafter. Patients with HF were older, more likely female, had more comorbidities, and were less likely to receive effective cardiac medications compared with patients without HF. The multivariable adjusted odds for in-hospital death were higher for patients with HF at presentation and thereafter (3.1 and 5.5, respectively) than those without HF. CONCLUSIONS: Results from this nationwide registry suggest that the incidence and hospital death rates associated with HF complicating AMI remain high. Patients developing HF after hospital admission are at even greater risk than those presenting with HF. Effective cardiac therapies remain underutilized in these patients, and the reasons for this underutilization need to be explored.

Aged↗