Optimal Heart Rate Research Articles

RAte Control Efficacy in permanent atrial fibrillation: a comparison between lenient versus strict rate control in patients with and without heart failure. Background, aims, and design of RACE II

Recent studies demonstrated that rate control is an acceptable alternative for rhythm control in patients with persistent atrial fibrillation (AF). However, optimal heart rate during AF is still unknown. To show that in patients with permanent AF, lenient rate control is not inferior to strict rate control in terms of cardiovascular mortality, morbidity, neurohormonal activation, New York Heart Association class for heart failure, left ventricular function, left atrial size, quality of life, and costs. The RACE II study is a prospective multicenter trial in The Netherlands that will randomize 500 patients with permanent AF (< or = 12 months) to strict or lenient rate control. Strict rate control is defined as a mean resting heart rate < 80 beats per minute (bpm) and heart rate during minor exercise < 110 bpm. After reaching the target, a 24-hour Holter monitoring will be performed. If necessary, drug dose reduction and/or pacemaker implantation will be performed. Lenient rate control is defined as a resting heart rate < 110 bpm. Patients will be seen after 1, 2, and 3 months (for titration of rate control drugs) and yearly thereafter. We anticipate a 25% 2.5-year cardiovascular morbidity and mortality in both groups. Enrollment started in January 2005 in 29 centers in The Netherlands and is expected to be concluded in June 2006. Follow-up will be at least 2 years with a maximum of 3 years. This study should provide data how to treat patients with permanent AF.

Multislice Spiral Computed Tomography for the Evaluation of Stent Patency After Left Main Coronary Artery Stenting

Surveillance conventional coronary angiography (CCA) is recommended 2 to 6 months after stent-supported left main coronary artery (LMCA) percutaneous coronary intervention due to the unpredictable occurrence of in-stent restenosis (ISR), with its attendant risks. Multislice computed tomography (MSCT) is a promising technique for noninvasive coronary evaluation. We evaluated the diagnostic performance of high-resolution MSCT to detect ISR after stenting of the LMCA. Seventy-four patients were prospectively identified from a consecutive patient population scheduled for follow-up CCA after LMCA stenting and underwent MSCT before CCA. Until August 2004, a 16-slice scanner was used (n = 27), but we switched to the 64-slice scanner after that period (n = 43). Patients with initial heart rates > 65 bpm received beta-blockers, which resulted in a mean periscan heart rate of 57 +/- 7 bpm. Among patients with technically adequate scans (n = 70), MSCT correctly identified all patients with ISR (10 of 70) but misclassified 5 patients without ISR (false-positives). Overall, the accuracy of MSCT for detection of angiographic ISR was 93%. The sensitivity, specificity, and positive and negative predictive values were 100%, 91%, 67%, and 100%, respectively. When analysis was restricted to patients with stenting of the LMCA with or without extension into a single major side branch, accuracy was 98%. When both branches of the LMCA bifurcation were stented, accuracy was 83%. For the assessment of stent diameter and area, MSCT showed good correlation with intravascular ultrasound (r = 0.78 and 0.73, respectively). An intravascular ultrasound threshold value > or = 1 mm was identified to reliably detect in-stent neointima hyperplasia with MSCT. Current MSCT technology, in combination with optimal heart rate control, allows reliable noninvasive evaluation of selected patients after LMCA stenting. MSCT is safe to exclude left main ISR and may therefore be an acceptable first-line alternative to CCA.

Pitfalls, artifacts, and remedies in multi- detector row CT coronary angiography.

Coronary angiography is increasingly performed with multi-detector row computed tomography (CT) in the clinical setting. Successful use of this method, however, depends on the radiologist's knowledge of its potential pitfalls and familiarity with methods for minimizing or avoiding them. To identify artifacts and other pitfalls that commonly degrade image quality and that could result in misinterpretation, contrast-enhanced coronary angiograms acquired with a multi-detector row CT scanner with four detector rows in 110 consecutive patients were analyzed. The problems identified were classified into four broad categories: (a) motion-related artifacts caused by cardiac, pulmonary, or other body motion; (b) beam-hardening effects caused by metallic implants, severe calcifications, or air bubbles in the pulmonary artery that obscured the underlying coronary vessel lumen; (c) structural artifacts produced by adjacent contrast material-filled structures and overlying vessels; and (d) artifacts that resulted from technical errors or limitations. The most frequently observed artifacts were those related to cardiac motion. The most effective methods for minimizing cardiac motion artifacts are (a) premedication with beta-blockers to maintain optimal heart rate during scanning and (b) optimal selection of the reconstruction window.

Circadian rhythm of the corrected QT interval: impact of different heart rate correction models.

A reduced circadian pattern in the QTc interval has been repeatedly reported to provide prognostic information in cardiac patients. However, the results of studies in healthy subjects in which different heart rate correction formulas were used are inconsistent regarding the presence and extent of diurnal variations in QTc. This study compared the diurnal variations in QTc obtained with four frequently used heart rate correction models with those based on individually optimized heart rate correction. In 53 subjects (25 men aged 27 +/- 7 years and 28 women aged 27 +/- 9 years) 12-lead digital ECGs were obtained every 30 seconds during 24 hours. The QT interval was measured automatically by six different algorithms provided by a commercially available device. The QT/RR relation was estimated by four common heart rate correction models and by an individually optimized correction model, QTc = QT/RR alpha. In each 24-hour recording, RR, QT, and WTc intervals of separate ECG samples were averaged over 10-minute intervals. Marked differences were found in the extent of the circadian pattern of QTc obtained with different formulas for heart rate correction. Under and overcorrection of the QT interval resulted in significant over- or underestimation of the circadian pattern. Thus, the extent of circadian variation in QTc depends highly on the heart rate correction formula used. To obtain proper insight regarding diurnal variation in QTc prolongation during pharmacologic therapy and/or to assess higher risk due to impaired autonomic regulation of ventricular repolarization, individualized heart rate correction is necessary.

Defining the optimum upper heart rate limit during exercise: a study in pacemaker patients with heart failure.

There is no non-invasive method to determine the individual optimum of maximum exercise heart rate. Knowledge of this value is of particular interest in patients with structural heart disease who are prone to tachycardia intolerance. The purpose of this study was to define the optimal maximum heart rate using cardiopulmonary exercise testing and exercise Doppler echocardiography and to compare the results of both approaches. In 49 pacemaker patients with chronotropic incompetence, the optimum upper heart rate limit was determined using cardiopulmonary exercise testing and exercise Doppler echocardiography. The optimum upper rate limit was given by the highest pacing rate which still produced an increase in oxygen consumption, or by that pacing rate which was linked to the lowest value for the Doppler-derived myocardial performance index. In patients with normal left ventricular ejection fraction (>or=55%) the optimum upper rate limit was 86% of age-predicted maximum heart rate, in patients with left ventriuclar dysfunction (ejection fraction <or=45%) it was 75% of the age-predicted maximum rate (P=0.004). The optimum upper rate limit, as defined by cardiopulmonary exercise testing and exercise Doppler echocardiography, were closely correlated (P<0.0001) with a mean deviation of 6+/-6 beats x min(-1). Cardiopulmonary exercise testing and exercise Doppler echocardiography are valuable tools which help to determine the optimum upper rate limit in order to avoid excess heart rates in heart failure patients. The application of these methods is not limited to pacemaker patients but may be helpful in therapeutic interventions with chronotropic drugs.

New concepts in diastolic dysfunction and diastolic heart failure: Part II: causal mechanisms and treatment.

As described in Part I of this 2-part article,1 diastolic heart failure is common and causes significant alterations in prognosis. In Part II, experimental studies that have provided insight into the mechanisms that cause diastolic heart failure will be described.2–19⇓⇓⇓⇓⇓⇓⇓⇓⇓⇓⇓⇓⇓⇓⇓⇓⇓ In addition, current treatment strategies and the design of future clinical trials of diastolic heart failure will be discussed. The development of truly effective therapy for diastolic heart failure depends on gaining a clear understanding of the basic mechanisms that alter diastolic function and the ability to efficiently target these mechanisms to correct these abnormalities in diastolic function. Conceptually, the mechanisms that cause abnormalities in diastolic function that lead to the development of diastolic heart failure can be divided into factors intrinsic to the myocardium itself (myocardial) and factors that are extrinsic to the myocardium (extramyocardial; Table 1). Myocardial factors can be divided into structures and processes within the cardiac muscle cell (cardiomyocyte), within the extracellular matrix (ECM) that surrounds the cardiac muscle cell, and that activate the autocrine or paracrine production of neurohormones. Each of these mechanisms are active in the major pathological processes that result in diastolic dysfunction and heart failure. Myocardial and extramyocardial mechanisms, cellular and extracellular mechanisms, and neurohumoral activation each play a role in the development of diastolic heart failure caused by ischemia, pressure-overload hypertrophy, and restrictive and hypertrophic cardiomyopathy. View this table: Table 1105290. Diastolic Heart Failure: Mechanisms ### Cardiomyocyte Diastolic dysfunction can be caused by mechanisms that are intrinsic to the cardiac muscle cells themselves. These include changes in calcium homeostasis caused by (1) abnormalities in the sarcolemmal channels responsible for short- and long-term extrusion of calcium from the cytosol, such as the sodium calcium exchanger and the calcium pump; (2) …

Quantitative Analysis of Cardiac Data from Rats Monitored by Telemetry: Reducing Within- and Between-Animal Variability

Few studies have examined the sources of variability in cardiac function measurements in unrestrained animals and the impact of this variability on detection of treatment effects. The heart rate was monitored with implanted ECG transmitters in two groups of male rats, age 7 and 23 mo. Animals were monitored in their cages to determine optimal heart rate sampling frequency and sources of variability in heart rate, including whether there were persistent animal-to-animal differences. Ambient temperature was transiently increased to test whether correction for animal-to-animal differences improved sensitivity for detection of treatment effects. Animal-to-animal differences were statistically significant and accounted for about 18.3% and 11.5% of the total variance for old and young rats, respectively. In both the old and young rats, the heart rate decreased during the heat challenges relative to the control group, but the noncorrected differences were not statistically significant. When pre-exposure baseline values for each rat (average of 72 h prior to the first temperature challenge) were subtracted, the decrease in heart rate was statistically significant during all three challenges for both old and young rats. Subtraction of preexposure heart rate data to correct for baseline differences between animals is important for measuring treatment effects.

Optimal target heart rate for exercise-induced T-wave alternans.

This study was conducted to determine the optimal target heart rate (HR) for the use of exercise-induced T-wave alternans (TWA) as an index for risk of malignant ventricular tachyarrhythmias. Rate-dependent TWA is an index of vulnerability to ventricular tachyarrhythmias. However, false positive TWA was reported to occur in normal subjects at high HR. Two groups were evaluated: Group I: 50 patients with malignant ventricular tachyarrhythmias, who received an implantable cardioverter-defibrillator (ICD); and Group II: 55 age-matched normal subjects. In both Groups, TWA was evaluated during symptom-limited bicycle exercise test. Peak HR during exercise test was 103 +/- 17 beats/min in Group I, versus 124 +/- 18 beats/min in Group II (P < 0.001). In Group I, 4 patients were excluded from analysis, due to high noise level or frequent ectopy during exercise. Out of the remaining 46 patients, TWA was present in 28 patients (61%), and absent in 18 (39%). In group II, TWA was present in four subjects (7%), and absent in 51 (93%). HR at the onset of TWA was 91 +/- 11/min in Group I, and 119 +/- 12/min in Group II (P < 0.001). Receiver operated characteristics curves demonstrated that a HR of 115 beats/min was the cutoff with the best sensitivity and specificity for TWA (100 and 96%, respectively). None of the patients in Group I developed TWA at HR > 115 beats/min, while two out of four in Group II had TWA at HR > 115/minutes. However, 13 patients in Group I who had no TWA were unable to exercise to a peak HR > 115 beats/min, compared to nine subjects in Group II. A target HR of 115 beats/min was highly sensitive and specific for determination of exercise-induced TWA as an index of risk of malignant ventricular tachyarrhythmias. However, a significant number of patients may not be able to achieve this target HR, resulting in an indeterminate test. The value of pharmacologic testing in this group should be assessed.

Effect of Heart Rate on T Wave Alternans

T wave alternans (TWA) is a promising technique for detecting arrhythmia vulnerability. Previous studies in animals demonstrated that the magnitude of TWA is dependent on heart rate. However, the effects of heart rate on TWA in humans and the clinical relevance of this effect remain controversial. This was a prospective evaluation of pacing rate and monitoring lead configuration on TWA in subjects undergoing electrophysiologic study. Measurements of TWA were performed on 45 patients in the absence of antiarrhythmic drugs. Recordings were made in normal sinus rhythm and during atrial pacing at 100 and 120 beats/min. Sustained monomorphic ventricular tachycardia (VT) was induced in 29 patients with programmed stimulation. TWA in the vector magnitude lead increased with heart rate, independent of VT inducibility (0.4 +/- 0.7 microV, 1.6 +/- 1.9 microV, and 2.4 +/- 2.1 microV in sinus rhythm and at 100 and at 120 beats/min, respectively; P < 0.001). In addition, the diagnostic performance of TWA for inducible VT was dependent on heart rate (sensitivity 4%, 42%, and 65%, and specificity 100%, 93%, and 63% at 77, 100, and 120 beats/min, respectively). By analyzing orthogonal leads rather than the vector magnitude lead, the sensitivity is increased from 42% to 59% at 100 beats/min, but the specificity is reduced from 93% to 72%. These results indicate that TWA in humans is strongly dependent on heart rate with regard to both magnitude and diagnostic performance. The optimal heart rate for the measurement of TWA is between 100 and 120 beats/min and multiple leads should be monitored.

A robust sensor fusion method for heart rate estimation.

Physiologic data measured in the clinical environment is frequently corrupted causing erroneous data to be displayed, periods of missing information or nuisance alarms to be triggered. To date, the possibility of combining sensors with similar information to improve the quality of the extracted data has not been developed. The objective of this work is to develop a method for combining heart rate measurements from multiple sensors to obtain: (i) an estimate of heart rate that is free of artifact; (ii) a confidence value associated with every heart rate estimate which indicates the likelihood that an estimate is correct; (iii) a more accurate estimate of heart rate than is available from any individual sensor. The essence of the method is to discriminate between good and bad sensor measurements and combine only the good readings to derive an optimal heart rate estimate. Past estimates of heart rate are used to derive a predicted value for the current heart rate that is also fused along with the sensor measurements. Consensus between sensor measurements, the predicted value and physiologic credibility of the readings are used to distinguish between good and bad readings. Three sensor measurements and the predicted value are evaluated yielding 16 possible hypotheses for the current state of the available data. A Kalman filter uses the most likely hypothesis to derive the fused estimate. Statistical measures of the sensor error and rate of change of heart rate are adaptively estimated when data are sufficiently reliable and used to enhance the hypothesis selection process. The method of sensor fusion presented has been documented to perform well using clinical data. Limitations of the technique and the assumptions employed are discussed as well as directions for future research.

Heart-rate-proportional oxygen consumption for constant cardiac work in dog heart.

We studied whether there is an optimal heart rate (HR) that would minimize myocardial oxygen consumption (MVO2) per min for a constant minute cardiac work. We measured minute MVO2 (ml O2/min) of the left ventricle paced at increasing rates (100-200 beats/min) in 10 right-heart-bypassed dogs. In each experiment, cardiac output was kept constant with a constant-flow bypass pump, and mean aortic pressure was also kept constant by inflation or deflation of an intra-aortic balloon. Minute cardiac work was thus kept constant. Minute MVO2 was obtained as the product of mean coronary arteriovenous O2 difference and mean coronary blood flow drained from the collapsed right ventricle. Both left ventricular Emax (contractility index defined as the slope of the left ventricular end-systolic pressure-volume relation) and PVA (pressure-volume area as a measure of total mechanical energy of contraction) were obtained by an abrupt aortic occlusion method. The obtained-minute MVO2-HR relationship showed a good linear positive correlation (r = 0.824-0.995) in every heart. We accounted for this relationship by the changes in PVA and Emax that we had proposed as primary determinants of MVO2. We conclude that minute MVO2 for a constant minute cardiac work increased monotonically with increases in HR from 100 to 200 beats/min, being minimum at the lowest HR, and that this relation was ascribable to the HR-proportional increase in the MVO2 component for the excitation-contraction coupling.

Central body temperature as a guide to optimal heart rate.

Studies in man suggest that fixed-rate artificial pacemakers do not return hemodynamic function to normal, since the principal mechanism for the increase in cardiac output with exercise, increased heart rate, is not restored. Special pacemakers are available that can detect atrial activity and pace the ventricles in coordination, but nearly half of the patients receiving artificial pacemakers have abnormal atrial function (atrial fibrillation, sick sinus syndrome). This study examined the effects of exercise on the temperature of blood returning to the right atrium. Precision thermistors, placed in the right hearts of conscious dogs, recorded temperature increases of 1 degree C (range 0.4-1.5 degrees C) during submaximal treadmill exercise. Temperature change correlated well with work load and changes in heart rate.

Hemodynamic changes following ventricular aneurysmectomy during the first three postoperative days.

One hundred twenty-eight patients underwent left ventricular aneurysmectomy; in 78 cases the procedure was combined with either aortocoronary bypass or valve replacement. In 7 patients undergoing isolated aneurysmectomy the influence of atrial pacing on various hemodynamic parameters was studied immediately postoperatively and on the first, second and third postoperative days. Until a certain point, increase in heart rate resulted in decrease of left ventricular filling pressure and increase of cardiac output, while systemic pressure changed only slightly. For each patient and each day the optimal heart rate as well as the optimal point of the Starling curve in these patients was found at extremely low filling pressures Kirklin's scheme of therapy may be limited in these patients. Therefore, in low cardiac output syndrome, left ventricular filling pressure should only be increased after the optimal heart rate is selected by atrial stimulation.

Cardiac performance: optimal heart rate for maximal cardiac output.

To determine optimal heart rate for the maximal cardiac output at various levels of inotropy and blood volume, the relationship between heart rate (HR) and stroke volume (SV) was examined in anaesthetized dogs during right atrial pacing. Myocardial inotropy was raised by intravenous infusion of isoproterenol, a stimulator of adrenergic beta-receptors, and reduced by propranolol, an inhibitor of adrenergic beta-receptors. Circulating blood volume was increased by saline infusion. Within the range of optimal heart rate, SV and HR were inversely related: SV = k (HR0-HR), where k indicates the relationship between changes in SV and HR. The intercept with the HR axis is HR0. At constant HR a rise in inotropy increased SV and a fall in inotropy reduced SV. These changes in SV were eual at every HR, and k was therefore constant. In contrast, blood volume expansion increased SV more at low than at high HR (k increased), but HR0 was not significantly changed. Calculated maximal cardiac output: k.HR02/4, and optimal heart/rate: HR0/2, agreed with observations when maximal cardiac output was raised from 1900 to 4500 ml/min by increasing blood volume and inotropy. Optimal HR was not influenced by changes in blood volume, but was increased from 160 to 200 beats/min by increasing inotropy. We conclude that the optimal heart rate and the maximal cardiac output can be predicted from the linear relationship between SV and HR during right atrial pacing.

(I) A Comparison of Cardiac Output Measured by Impedance and Other Tests, and Determination of Optimal Heart Rate in Atrial Fibrillation : Studies on Transthoracic Electrical Impedance

(I) A Comparison of Cardiac Output Measured by Impedance and Other Tests, and Determination of Optimal Heart Rate in Atrial Fibrillation : Studies on Transthoracic Electrical Impedance

Effect of heart rate on zonal tension and ischaemia following coronary occlusion: optimal rate for Treppe versus ischaemia.

The optimal heart rate in the immediate period following acute coronary occlusion has been controversial from the standpoint of arrhythmias and the extent of ischaemic injury. In the present study we have examined the effect of heart rate on both local myocardial contractile ability and ischaemia in 10 open chested dogs using strain gauge arches and epicardial electrograms. After sinus node destruction, atrial pacing was instituted for rate control at 100/min and increased randomly to 150, 175, and 200/min. Before coronary occlusion, total tension and rate of tension rise progressively increased at higher rates while ST segments demonstrated no significant changes. After coronary artery occlusion, total tension and rate of tension rise in the ischaemic zone decreased markedly and showed no significant change with increments in pacing rate. In the border zone, after the initial decrease in tension, pacing at 150 beats/min improved tension without a change in ST segments. However, when the rate was increased to 175 and 200 beats/min, although border zone tension increased further, ST segments rose significantly. Thus, a heart rate between 100-150/min provides the optimal range for increasing contractile ability in the nonischaemic and border zones without adversely affecting the degree of ischaemic injury.

Thermodilution cardiac output measurement in infants and small children following intracardiac surgery

A modified catheter has been used in conjunction with a thermodilution cardiac output computer for postoperative assessment of cardiac function in infants and children. Because of the small amount of fluid required for each determination and the simplicity of the technique, serial measurements can be done safely. Its use has a contributed to the early detection of low output states. It has also proven to be a useful tool for estimating the optimal heart rate in each patient and for assessing the effectiveness of therapeutic measures.

Pacing studies after cardiac surgery.

The diagnostical use of pacemaker after cardiac surgery is presented. Temporary pacemaker electrodes have been inserted during surgery into the wall of atrial and ventricular myocardium. With the aid of these electrodes, an analysator wire of 6 volts, and a Medtronic 5840 type pacemaker electrophysiological studies have been performed. The diastolic and supernormal stimulation threshold, the duration of atrial and ventricular relative refractory period were measured, the clinical significance of latency was analysed. It has been found that decrease of stimulation threshold, shortening of relative refractory period, and appearance of latency phenomenon promote arrhythmias. By investigating the conduction capacity of atrioventricular conduction system, latent conduction disturbances could be revealed, and a significant difference could be demonstrated between the atrioventricular conduction of WPW syndrome and that of other kinds of PR interval shortening. In addition the optimal heart rate requirement (optimal pacing rate) following heart surgery was defined. These parameters present more precise information on the electrophysiological condition of the heart than does the generally used ECG monitoring. When these parameters are repeatedly determined, the significance of patient's arrhythmias can be evaluated more safely and accurately; in a number of cases, even in the absence of any rhythm disturbances, impending arrhythmias can be predicted. "Pacemaker monitoring" of the postoperative heart patients, therefore, affords greater possibility for preventing the development of major cardiac arrhythmias.

Sequential circulatory changes following acute myocardial infarction in man. Determination of optimal heart rate at each stage of the infarction by atrial pacing.

After informed consent, 12 men with documented acute myocardial infarction had hemodynamic studies performed within 18 hours after onset of symptoms. These were repeated on the second day, at 3-5 weeks, and at 3-5 months in the 10 who survived. One half of the patients were "uncomplicated" and significant differences with the "complicated" patients were seen in pulmonary artery pressure, mean arterial pressure on the first day, acute phase stroke volume and cardiac index, and the total blood volume within 48 hours. The optimal heart rate at each stage was determined by atrial pacing and was found to be 110 ± 10 beats/min. Abnormalities in p H, blood gases, and circulation time were related to the cardiac index. Control groups with and without coronary artery disease were studied prior to angiography to obtain information regarding preinfarction circulatory status, and significant impairment of the ejection fraction was noted even in angina patients without prior infarction. The sequential circulatory changes and possible compensatory mechanisms available were discussed.