Images in cardiology: Rare case of pericarditis constrictiva.
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Aged↗
Biomedical subjects
D Weilenmann
Publications and source records attributed to D Weilenmann.
Clinical evaluation of a pacemaker algorithm that adjusts the pacing rate during sleep using activity variance.
Even though rate responsive pacemakers are able to regulate pacing rates based on sensor activity, they are set with a minimum rate that is not adjusted to provide rate decreases during sleep. The aim of this study was to evaluate the performance of the "Sleep Rate" feature, as compared to patient diaries and a validated method that identifies sleep from wrist actigraphy. In 19 patients (15 men; age 69 +/- 8 years) with Pacesetter Trilogy DR+ pacemakers, the base rate and the sleep rate were set to 80 and 50 ppm, respectively. When the patients returned 2 days later, data recorded by the pacemaker and wrist actigraph were analyzed to find the agreement in corresponding sleep/wake periods. In 17 (89%) patients, the pacemaker went into the sleep mode. The total sleep time derived from actigraphy significantly exceeded the time during which the pacemaker was in sleep mode (1156.8 +/- 83.4 vs 307.3 +/- 77.2 minutes). Frequent reversions out of the sleep mode limited the total sleep time derived from the pacemaker. Cumulative analysis of the pacemaker data showed that the maximum time in the sleep mode was 78 minutes, and exceeded 1 hour in six instances, 30 minutes in 32 instances, and 15 minutes in 83 instances. Epoch by epoch comparisons revealed a good agreement (93.6 +/- 1.8%) during wakefulness between the corresponding actigraph and pacemaker epochs. However, only 24.6 +/- 3.7% of the corresponding epochs during sleep were identical, and the overall agreement was 54.4 +/- 3.7%. Except for one patient who reported palpitations, patients did not suffer from a pacemaker rate change. The Sleep Rate feature provides rate reduction during sleep, while assuring rapid frequency response during physical activity. However, the current algorithm does not allow long periods of slow pacing rate during continuous sleep, possibly due to its conservative design and the presence of movement arousals, which has to be improved in future generation algorithms.
Aged↗
Importance of ventricular rate after mode switching during low intensity exercise as assessed by clinical symptoms and ventilatory gas exchange.
Automatic mode switching from DDD(R) to DDI(R) or VVI(R) pacing modes has improved dual chamber pacing in patients at high risk for supraventricular tachyarrhythmias. However, little is known about the effect of ventricular pacing rate adaptation after mode switching. We conducted a single-blinded, crossover study in 15 patients (58 +/- 21 years) with a DDD pacemaker who had AV block and normal sinus node function to investigate the influence of pacing rate adaptation to intrinsic heart rate during low intensity exercise. Patients performed two tests (A/B) of low intensity treadmill exercise (0.5 W/kg) in randomized order. They initially walked for 6 minutes while paced in DDD mode. The pacing mode was then switched to VVI with a pacing rate of either 70 beats/min (test A) or matched to the intrinsic heart rate (95 +/- 11 beats/min test B). Respiratory gas exchange variables were determined and patients classified the effort before and after mode switching on a Borg scale from 6 to 20. Percentage changes of respiratory gas exchange measurements were significantly larger (O2 consumption: -8.2 +/- 5.0% vs. -0.6 +/- 7.2%; ventilatory equivalent of CO2 exhalation: 5.3 +/- 4.9% vs. 1.5 +/- 4.3%; respiratory exchange ratio: 7.0 +/- 2.2% vs. 3.5 +/- 3.0%; end-tidal CO2: -5.7 +/- 2.9% vs. -1.8 +/- 2.7%; all P < 0.01) and the increase in subjective assessment of the effort tended to be higher (mean increase on Borg scale: 1.6 +/- 1.9 vs. 1.1 +/- 1.8, P = 0.07) after heart rate unadjusted than after adjusted mode switching. Mode switching from DDD to VVI pacing is better tolerated and gas exchange measurements are less influenced if ventricular pacing rate is adjusted to the level of physical activity. Thus, pacing rate adjustment should be considered as part of automatic mode switch algorithms.
Adolescent↗
Influence of acute exposure to high altitude and hypoxemia on ventricular stimulation thresholds in pacemaker patients.
Cardiac stimulation threshold of implanted pacemakers may be influenced by a variety of endogenous and exogenous factors. High altitude provokes hypoxemia, which may change stimulation thresholds, besides causing other important physiological changes. The aim of our study was to investigate the influence of high altitude on ventricular stimulation thresholds in pacemaker patients. Thirteen patients (10 men; aged 65.5 +/- 4.8 years) with implanted single chamber pacemakers (nine with Pacesetter Regency SR+ with the Autocapture feature) were exposed to an altitude of 4,000 m above sea level, as simulated in a hypobaric chamber. Stepwise ascension was performed with a speed of 5 m/s starting at 450 m above sea level. A 5-minute rest was performed every 500 m to measure stimulation threshold at each step. After a stay of 30 minutes at 4,000 m stimulation threshold was measured, followed by a stepwise descent. Pacemaker interrogation and arterial blood gas analysis were performed at 450 and at 4,000 m, and a strength-duration curve was determined. Blood pressure, heart rate, and oxygen saturation were monitored continuously during the study. Ascent to 4,000 m above sea level induced a significant decrease in arterial pO2 (10.7 +/- 1.1 vs 5.5 +/- 0.3 kPa), pCO2 (5.3 +/- 0.3 vs 4.7 +/- 0.4 kPa), oxygen saturation measured by arterial blood gas analysis (95.5% +/- 1.2% vs 79.1% +/- 2.5%), and increase in pH (7.39 +/- 0.02 vs 7.45 +/- 0.04) (P < 0.0001). Stimulation thresholds and the strength-duration curve remained unchanged in all patients throughout the study. In conclusion, exposure to an altitude of 4,000 m above sea level with resultant hypobaric hypoxemia has no impact on ventricular stimulation thresholds. Therefore, in regard to the safety of pacing, pacemaker patients can safely be exposed to this altitude.
Acute Disease↗
Prognostic significance of oxygen uptake kinetics during low level exercise in patients with heart failure.
Oxygen uptake kinetics during low-intensity exercise were investigated in 48 patients with congestive heart failure to assess their prognostic value compared with established predictors of prognosis including neurohumoral stimulation. Mean response time of oxygen uptake during low-intensity exercise, which does not require the patient's maximal effort, appears to be an important predictor of prognosis in these patients.
Adult↗
Within-patient comparison of effects of different dosages of enalapril on functional capacity and neurohormone levels in patients with chronic heart failure.
BACKGROUND: Angiotensin-converting enzyme (ACE) inhibitors are established as first-line therapy in chronic heart failure (CHF). However, conflicting results exist regarding the dose-effect relation of ACE inhibitors. METHODS: We investigated 45 patients (age 55 +/- 10 years) with stable CHF who presented with a maintenance dosage of enalapril of either 5 mg given twice daily (E10; n = 16), 10 mg given twice daily (E20; n = 18), or 20 mg given twice daily (E40; n = 11). This dosage was changed 3 times to treat all patients with lower, higher, and the initial dosages for 4 weeks each. Neurohormones (atrial natriuretic peptide [ANP], brain natriuretic peptide [BNP], and norepinephrine) and enalaprilat trough levels were measured, and ergospirometry was performed. RESULTS: Changes in enalapril dose and enalaprilat level were concordant in 82% of patients, indicating good compliance. After augmentation of enalapril to 40 mg daily, patients in the E10 group showed an increase in maximal oxygen consumption and a decrease in neurohormonal stimulation, whereas the opposite changes were observed after reduction of enalapril to 10 mg daily in patients in the E20 and E40 groups (maximal oxygen consumption: Delta1.1 +/- 2.0 vs -1.0 +/- 1.9 mL. kg(-1). min(-1), P <.01; ANP: Delta-63 +/- 106 vs 19 +/- 54 pg/mL, P <.01; BNP: Delta-62 +/- 104 vs 18 +/- 89 pg/mL, P <.05; norepinephrine: Delta-1.3 +/- 2.9 vs 0.6 +/- 1.8, P <.05). Within-patient comparison showed that neurohormone levels were higher and exercise capacity lower while patients were receiving 10 mg of enalapril per day than when they were receiving 40 mg per day (ANP: 172 +/- 148 vs 139 +/- 122 pg/mL, P <.01; BNP: 193 +/- 244 vs 152 +/- 225 pg/mL, P <.005; norepinephrine: 4.2 +/- 2.2 vs 3.5 +/- 1. 6 nmol/L, P <.05; maximal oxygen consumption 22.0 +/- 4.4 vs 21.3 +/- 4.3 mL. kg(-1). min(-1) P <.05). Similar differences were observed when comparing these variables, and patients had lowest and highest enalaprilat trough levels. CONCLUSIONS: High doses of enalapril resulted in an improvement of exercise capacity and reduction of neurohumoral stimulation, whereas these parameters worsened after reduction of enalapril dose. Thus patients with congestive heart failure may benefit from increasing dosage of ACE inhibitors.
Angiotensin-Converting Enzyme Inhibitors↗
Oxygen uptake kinetics during low level exercise in patients with heart failure: relation to neurohormones, peak oxygen consumption, and clinical findings.
OBJECTIVE: To investigate whether oxygen uptake (VO2) kinetics during low intensity exercise are related to clinical signs, symptoms, and neurohumoral activation independently of peak oxygen consumption in chronic heart failure. DESIGN: Comparison of VO2 kinetics with peak VO2, neurohormones, and clinical signs of chronic heart failure. SETTING: Tertiary care centre. PATIENTS: 48 patients with mild to moderate chronic heart failure. INTERVENTIONS: Treadmill exercise testing with "breath by breath" gas exchange monitoring. Measurement of atrial natriuretic factor (ANF), brain natriuretic peptide (BNP), and noradrenaline. Assessment of clinical findings by questionnaire. MAIN OUTCOME MEASURES: O2 kinetics were defined as O2 deficit (time [rest to steady state] x DeltaVO2 -sigmaVO2 [rest to steady state]; normalised to body weight) and mean response time of oxygen consumption (MRT; O2 deficit/DeltaVO2). RESULTS: VO2 kinetics were weakly to moderately correlated to the peak VO2 (O2 deficit, r = -0.37, p < 0.05; MRT, r = -0.49, p < 0.001). Natriuretic peptides were more closely correlated with MRT (ANF, r = 0.58; BNP, r = 0.53, p < 0.001) than with O2 deficit (ANF, r = 0.48, p = 0.001; BNP, r = 0.37, p < 0.01) or peak VO2 (ANF, r = -0.40; BNP, r = -0.31, p < 0.05). Noradrenaline was correlated with MRT (r = 0. 33, p < 0.05) and O2 deficit (r = 0.39, p < 0.01) but not with peak VO2 (r = -0.20, NS). Symptoms of chronic heart failure were correlated with all indices of oxygen consumption (MRT, r = 0.47, p < 0.01; O2 deficit, r = 0.39, p < 0.01; peak VO2, r = -0.48, p < 0. 01). Multivariate analysis showed that the correlation of VO2 kinetics with neurohormones and symptoms of chronic heart failure was independent of peak VO2 and other variables. CONCLUSIONS: Oxygen kinetics during low intensity exercise may provide additional information over peak VO2 in patients with chronic heart failure, given the better correlation with neurohormones which represent an index of homeostasis of the cardiovascular system.
Adult↗
Is blood pressure response to the Valsalva maneuver related to neurohormones, exercise capacity, and clinical findings in heart failure?
OBJECTIVES: To investigate the relationship of the BP response to the Valsalva maneuver (VM) to parameters of congestive heart failure (CHF) other than hemodynamic measures. DESIGN: Comparison of neurohormones (atrial natriuretic peptide [ANP], brain natriuretic peptide [BNP], norepinephrine [NE]), parameters of spiroergometry, and clinical parameters with BP response to the VM. SETTING: Tertiary care center. PATIENTS: Forty-five patients with stable CHF (ejection fraction, 28 +/- 7%). MEASUREMENTS: Pulse amplitude ratio (PAR) calculated between the end and the beginning of the VM using the last two and the first three beats of the straining phase. Failure of the systolic BP to fall below the resting level during the VM. RESULTS: Patients in the New York Heart Association class III (n = 15) had a higher PAR than those in class II (0.82 +/- 0.21 vs 0.63 +/- 0.20; p < 0.01). There was a close correlation between PAR and ANP (r = 0.76) and BNP (r = 0.62), whereas other parameters were less well correlated (eg, for peak f1.gif" BORDER="0">O(2), r = -0.35; p < 0.05). Patients with failure of the systolic BP to fall below the resting level (n = 24) had higher neurohormones (mean ANP, 246 +/- 158 vs 84 +/- 43 pg/mL; mean BNP, 282 +/- 289 vs 81 +/- 85 pg/mL; p < 0.001; mean NE, 3.9 +/- 1.7 vs 3.4 +/- 1.5 nmol/L; nanosecond), lower exercise capacity (19.8 +/- 5.2 vs 23.0 +/- 3.7 mL/kg/min; p < 0.05), and their quality of life (Minnesota questionnaire) was more compromised (31 +/- 19 vs 18 +/- 15; p < 0. 05). CONCLUSIONS: The BP response to the VM is related to a broad range of clinical and neurohumoral parameters of CHF. Whether or not it is also related to prognosis remains to be determined. Nevertheless, this easily applicable test should be part of the assessment of patients with CHF.
Adult↗
Plasma levels of enalaprilat in chronic therapy of heart failure: relationship to adverse events.
Angiotensin-converting enzyme (ACE) inhibitors are established as first-line therapy in chronic heart failure (CHF). However, little is known about the dosage-plasma-level relationship of ACE inhibitors in CHF and its relation to drug-induced adverse effects. We investigated 45 patients (age 55 +/- 10 years) with stable CHF who presented with a maintenance dosage of enalapril of either 5 mg b.i.d. (E10, n = 16), 10 mg b.i.d. (E20, n = 18), or 20 mg b.i.d. (E40, n = 11). This dosage was changed three times to treat all patients with lower, higher, and, finally, the initial dosage for 4 weeks each. Patients were examined clinically, by questionnaire, and by spiroergometry. In addition, neurohormones (atrial and brain natriuretic peptide and norepinephrine), enalaprilat trough levels, and serum potassium and creatinine were measured. Enalaprilat trough levels differed significantly between the three groups at study entry but also varied markedly within each group. In addition to the dose of enalapril, serum creatinine, severity of CHF, basal metabolic rate, and body weight significantly influenced enalaprilat trough levels (R2 =.84, p <.001). Within-patient comparisons revealed that serum creatinine (107 +/- 26 versus 102 +/- 20 micromol/liter) and potassium (3.8 +/- 0.4 versus 3.7 +/- 0. 3mmol/liter) were higher, cough was more common (scored on a scale of 0-8: 1.7 +/- 2.1 versus 1.4 +/- 1.8), and blood pressure was lower (systolic, 112 +/- 14 versus 117 +/- 13 mm Hg; diastolic, 66 +/- 9 versus 69 +/- 11 mm Hg) on the highest than on the lowest enalaprilat trough level (all p <.05). Highly variable enalaprilat trough levels and the fact that adverse effects were more common on high enalaprilat trough levels provide a rationale for individually adjusting ACE-inhibitor dose in case of adverse effects.
Adult↗
Activity-controlled circadian base rate.
The current pacing rates are clustered around a fixed base rate since pacemaker patients are usually sedentary, resting, or sleeping most of the time. This fixed base rate is either too low for daytime hemodynamic support or too high for nighttime rest and recovery. Multiple Holter studies involving normal individuals have suggested that the resting base rate fluctuates during the course of the day. The circadian base rate (CBR) algorithm was designed to provide patients with a circadian change in paced resting rate and a normal rate distribution. The CBR algorithm, using a sophisticated accelerometer sensor, was developed and tested using the downloaded activity data from patients implanted with Trilogy DR+ pacemakers. Twenty-five patients (19 men, 6 women, age 72 +/- 9 years) were studied. Trilogy DR+ is able to record the detailed sensor and system behavior data for a week. During outpatient visits, the pacemaker was interrogated and the data accumulated in the pacemaker memory were downloaded. The CBR algorithm was applied to the activity variance histogram to calculate the base rate and to construct its histogram. The base rates in the CBR histogram are generally below 100 ppm with a distribution that mimics the natural sinus rate distribution of normal subjects. The CBR algorithm provides the highest daytime rates for hemodynamic support and the lowest nighttime rates for cardiac recovery, with a smoothly changing base rate modeling the normal circadian variation in heart rate.
Aged↗
Relative frequency of functional sympathetic and parasympathetic reinnervation after heart transplantation.
Although there is evidence of partial sympathetic reinnervation late after transplantation, little is known about the relative frequency of sympathetic and, in particular, parasympathetic reinnervation. We examined the heart rate response to various maneuvers (standing up, handgrip exercise, phase 2 of Valsalva maneuver for sympathetic function, carotid sinus massage, phase 4 of Valsalva maneuver, and atropine for parasympathetic function) in 65 patients 3 to 110 months after transplantation and in 16 healthy volunteers and defined reinnervation as either one normal (>50% of control group) and at least one partial (>33% of control group) heart rate response or partial responses in all three tests of the respective part of the autonomic nervous system. Thirty-five (54%) patients had sympathetic reinnervation, but only 16 (25%) had parasympathetic reinnervation (p < 0.001); earliest reinnervation was found 11 months after transplantation, and all but one patient with parasympathetic reinnervation also had sympathetic reinnervation. Signs of sympathetic but not parasympathetic reinnervation were common late (>5 years) after transplantation (74% vs 30%).
Heart↗
Atrioventricular block after administration of atropine in patients following cardiac transplantation.
BACKGROUND: Atropine is widely used as a parasympatholytic agent during diagnostic and therapeutic procedures. We observed an unexpected paradoxical response to atropine after cardiac transplantation. METHODS: In a study investigating the occurrence of autonomic reinnervation after cardiac transplantation, atropine, at 0.015 mg/kg body weight, was given intravenously to 23 patients (mean age, 56+/-8 years) 98 days to 6.4 years after transplantation. RESULTS: Two patients experienced a witnessed syncope 40 and 150 min after administration of atropine. Second-degree atrioventricular (AV) block was documented in the first patient immediately afterward, and third-degree AV block was seen on 24-hr electrocardiogram monitoring in the second patient. A third patient developed documented AV block 15 min after atropine but experienced no sequelae because of a previously implanted pacemaker. CONCLUSIONS: Although the underlying mechanism is not clear, these findings suggest that atropine may paradoxically cause high-degree AV block in patients after transplantation. Accordingly, it should be used with caution and appropriate monitoring in these patients.
Adult↗