Beta-adrenergic Blockade Therapy Research Articles

Among Patients Taking Beta-Adrenergic Blockade Therapy, Use Measured (Not Predicted) Maximal Heart Rate to Calculate a Target Heart Rate for Cardiac Rehabilitation.

Among patients in cardiac rehabilitation (CR) on beta-adrenergic blockade (βB) therapy, this study describes the frequency for which target heart rate (THR) values computed using a predicted maximal heart rate (HR max ), correspond to a THR computed using a measured HR max in the guideline-based heart rate reserve (HR reserve ) method. Before CR, patients completed a cardiopulmonary exercise test to measure HR max , with the data used to determine THR via the HR reserve method. Additionally, predicted HR max was computed for all patients using the 220 - age equation and two disease-specific equations, with the predicted values used to calculate THR via the straight percent and HR reserve methods. The THR was also computed using resting heart rate (HR) +20 and +30 bpm. Mean predicted HR max using the 220 - age equation (161 ± 11 bpm) and the disease-specific equations (123 ± 9 bpm) differed ( P < .001) from measured HR max (133 ± 21 bpm). Also, THR computed using predicted HR max resulted in values that were infrequently within the guideline-based HR reserve range calculated using measured HR max . Specifically, 0 to ≤61% of patients would have had an exercise training HR that fell within the guideline-based range of 50-80% of measured HR reserve . Use of standing resting HR +20 or +30 bpm would have resulted in 100% and 48%, respectively, of patients exercising below 50% of HR reserve . A THR computed using either predicted HR max or resting HR +20 or +30 bpm seldom results in a prescribed exercise intensity that is consistent with guideline recommendations for patients in CR.

Beta-Adrenergic Blockade Therapy for Autonomic Dysfunction is Less Effective for Elderly Patients with Heart Failure and Reduced Left Ventricular Ejection Fraction.

OBJECTIVEHeart rate variability (HRV) has been reported to be an independent predictor of all-cause and sudden cardiac death in patients with heart failure. In the aging heart, however, both autonomic and cardiac functions appear to be altered. We assessed the relationship between aging and responsiveness of HRV and ventricular remodeling to beta-adrenergic blockade therapy in patients with heart failure and reduced ejection fraction (HFREF).METHODSTwenty-eight clinically stable patients with chronic heart failure, sinus rhythm, and left ventricular ejection fraction <50% as confirmed by echocardiography were included. At baseline and after carvedilol treatment, 24-hour ambulatory Holter monitor recording was used to analyze HRV indices by the maximum entropy method. Changes in these parameters were compared among three age groups.RESULTSHR decreased in all groups after carvedilol treatment, but was still highest in the youngest group despite the same treatment doses. Time and frequency domain variables improved. The response of time domain variables (the standard deviation of all normal sinus to normal sinus [NN] intervals and the standard deviation of the averages of NN intervals in all 5-minute or 30-minute segments) to carvedilol therapy significantly decreased with increasing age. Ventricular reverse remodeling induced by carvedilol therapy significantly decreased with increasing age. Increases in time domain variables and a low-frequency domain moderately correlated with left ventricular reverse remodeling.CONCLUSIONBeta-adrenergic blockade therapy improved HRV variables and ventricular remodeling in HFREF patients; however, the response tended to be milder in the elderly. HRV improvement was associated with ventricular reverse remodeling.

臨床 拡張型心筋症におけるβ遮断薬療法の有用性,適応と作用機序について

臨床 拡張型心筋症におけるβ遮断薬療法の有用性,適応と作用機序について

Identifying Target Heart Rate In Patients With Ischemic Heart Disease Without An Exercise Stress Test

Increasingly, patients enroll in cardiac rehabilitation without an exercise stress test, yet there are few evidence-based recommendations for establishing a target heart rate (HR) in this situation among patients with heart disease. PURPOSE In patients with ischemic heart disease, identify and compare the % of measured HR reserve when target HR is prescribed using resting HR plus 20 and at 65% of HR reserve calculated using a population-specific maximum HR prediction equation. METHODS We queried the Henry Ford Preventive Cardiology Outcomes (PRECO) database for patients with a history of myocardial infarction or revascularization procedure; preserved left ventricular function; age= 40–80 yr; sinus rhythm; and a graded treadmill test with a respiratory exchange ratio ≥1.10. Beginning May 2001, consecutive tests of 50 patients prescribed beta-adrenergic blockade (BB) therapy and 46 without BB were included. Percent measured HR reserve associated with resting HR plus 20 was calculated. HR at a moderate exercise intensity (65% HR reserve) was calculated using a predicted maximum HR [HRmax=164–0.72×Age (with BB) or HRmax=200–0.92×Age (no BB)]. RESULTS Mean % measured HR reserve based on resting HR plus 20 was 45±30% (mean±SD) and 31±12% for the BB and no BB patients, respectively. Mean % measured HR reserve using predicted maximum HR was 75±46% and 68±21% for the BB and no BB patients, respectively. Resting HR plus 20 resulted in a target HR that was < 40 % of measured HR reserve in 58% (29/50) of the patients on BB and 83% (38/46) of those without BB. Other results are shown in Table.TableCONCLUSIONS Among patients with ischemic heart disease: 1) A target HR based on resting HR plus 20 results in a suboptimal exercise intensity (< 40 % HR reserve) in over half of the patients, independent of the presence of BB therapy. 2) Target HR calculated at a moderate exercise intensity (65% HR reserve), using a population-specific maximum HR prediction equation, results in an exercise intensity that is within 50–85% measured HR reserve in 58% of the patients on BB and 72% the patients without BB.

Identifying Target Heart Rate In Patients With Ischemic Heart Disease Without An Exercise Stress Test

Increasingly, patients enroll in cardiac rehabilitation without an exercise stress test, yet there are few evidence-based recommendations for establishing a target heart rate (HR) in this situation among patients with heart disease. PURPOSE In patients with ischemic heart disease, identify and compare the % of measured HR reserve when target HR is prescribed using resting HR plus 20 and at 65% of HR reserve calculated using a population-specific maximum HR prediction equation. METHODS We queried the Henry Ford Preventive Cardiology Outcomes (PRECO) database for patients with a history of myocardial infarction or revascularization procedure; preserved left ventricular function; age= 40–80 yr; sinus rhythm; and a graded treadmill test with a respiratory exchange ratio ≥1.10. Beginning May 2001, consecutive tests of 50 patients prescribed beta-adrenergic blockade (BB) therapy and 46 without BB were included. Percent measured HR reserve associated with resting HR plus 20 was calculated. HR at a moderate exercise intensity (65% HR reserve) was calculated using a predicted maximum HR [HRmax=164–0.72×Age (with BB) or HRmax=200–0.92×Age (no BB)]. RESULTS Mean % measured HR reserve based on resting HR plus 20 was 45±30% (mean±SD) and 31±12% for the BB and no BB patients, respectively. Mean % measured HR reserve using predicted maximum HR was 75±46% and 68±21% for the BB and no BB patients, respectively. Resting HR plus 20 resulted in a target HR that was < 40 % of measured HR reserve in 58% (29/50) of the patients on BB and 83% (38/46) of those without BB. Other results are shown in Table.TableCONCLUSIONS Among patients with ischemic heart disease: 1) A target HR based on resting HR plus 20 results in a suboptimal exercise intensity (< 40 % HR reserve) in over half of the patients, independent of the presence of BB therapy. 2) Target HR calculated at a moderate exercise intensity (65% HR reserve), using a population-specific maximum HR prediction equation, results in an exercise intensity that is within 50–85% measured HR reserve in 58% of the patients on BB and 72% the patients without BB.

PERCENT HEART RATE RESERVE IS EQUIVALENT TO PERCENT VO2 RESERVE IN PATIENTS WITH HEART FAILURE

Previous studies show that % heart rate reserve (HRR) is equivalent to % VO2 reserve (VO2R) in healthy subjects (Swain, et al.) and those with prior myocardial infarction (Brawner, et al.). This study tested the hypothesis that % HRR is equivalent to % VO2R in patients with heart failure (HF) due to left ventricular systolic dysfunction. We queried the Henry Ford PREventive Cardiology Outcomes (PRECO) database for patients with HF, ejection fraction ≤ 35%, sinus rhythm and an inaugural, symptom-limited graded treadmill test with gas exchange performed between 8/1/1998 and 7/31/2000. Seventy-two patients were identified (46 males, 26 females; age = 53 ± 12 yr; EF = 22 ± 8%; VO2 = 16.5 ± 4 mL/kg/min; mean ± SD). Heart rate and VO2 data were collected continuously and averaged in 15s intervals. Linear regression was used to analyze the relationship of % HRR to % VO2R and % HRR to % VO2max. A mean slope and y-intercept was calculated for each regression line. T-tests were used to determine if either line was significantly different from a line of identity (slope = 1, y-intercept = 0) and if the two lines differed from each other. A sub-analysis examined the effect of beta-adrenergic blockade (BB) therapy on these relationships. Results: The mean slope and y-intercept for % HRR vs % VO2R was 0.97 ± 0.02 (mean ± SE) and −0.06 ± 0.02, respectively; not different from a line of identity. The relationship of % HRR vs % VO2max was significantly different from a line of identity (p ≤ 0.001), with a mean slope and y-intercept of 1.25 ± 0.03 and −0.34 ± 0.03, respectively. Seperate analyses for BB therapy did not change these results. Conclusion: Independent of BB therapy, in patients with HF due to left ventricular systolic dysfunction, exercise intensity should be based on % VO2R, not % VO2max.

Nifedipine in the treatment of unstable angina, coronary spasm and myocardial ischemia

The effects of nifedipine, a potent calcium antagonist, were studied in patients with unstable angina, coronary spasm and myocardial ischemia. Data from two separate groups of patients studied in the cardiac catheterization laboratory indicate that intracoronary injection of nifedipine promptly reversed coronary spasm—whether provoked or spontaneous—in five of six patients. In other patients, direct intracoronary injection of the drug was compared with intravenous administration. After intracoronary injection, local mechanical cardiac action virtually ceased, and the ventricular wall became thinner during systole. Thus, a specific inhibitory action on contractile energy expenditure could be demonstrated in the presence of increased coronary flow. This “oxygen-sparing” effect was tested in a group of 31 patients with symptomatic unstable angina whose pain at rest, with ST-T changes, had not responded to 8 hours of treatment with maximal beta adrenergic blockade, nitrates and bed rest. The addition of 6 × 10 mg of nifedipine rendered 27 of these patients asymptomatic within 1.5 hours. In the four patients who did not respond, coronary arteriography demonstrated severely stenotic lesions. Two of the four patients subsequently responded to intraaortlc balloon pumping and bypass surgery; one patient had a myocardial infarction and one who had a 90 percent reduction in the diameter of the left main coronary artery, died. It is concluded that nifedipine should be added to beta adrenergic blockade therapy if the latter does not appear to be immediately effective. This combination has not been shown to cause any hemodynamlc deterioration, and only a minority of the patients treated sustained a myocardial infarction during the first 3 months of follow-up. The use of nifedipine in unstable angina deserves further clinical evaluation.

Effects of chronic beta-adrenergic blockade therapy on exercise training in patients with coronary heart disease

Effects of chronic beta-adrenergic blockade therapy on exercise training in patients with coronary heart disease

Withdrawal of Antihypertensive Therapy

Hypertensive crises were reported in three patients with hypertension associated with underlying renovascular occlusive disease during reduction of antihypertensive therapy. In each case, rebound hypertension was observed during clonidine hydrochloride withdrawal. Therapy with propranolol hydrochloride and diuretics had also been discontinued in two of the three patients. This and other reports of rebound hypertension during clonidine withdrawal are contrasted with the absence of reports of this syndrome in the setting of cessation of beta-adrenergic blockade therapy. This suggests that the discontinuation of clonidine therapy was primarily responsible for the hypertensive crises herein described. It is further concluded that rebound hypertension may follow gradual as well as abrupt reduction of clonidine dosage, and that patients with renovascular hypertension may be at greatest risk.

Propranolol and surgical anesthesia.

The potential danger of anesthetizing a patient on beta-adrenergic blockade therapy has long been recognized. The cases of 73 patients taking propranolol and anesthetized for non-cardiac operations were reviewed with regard to preoperative administration of propranolol and intraoperative and postoperative complications. Of these patients, 72 percent took propranolol to within 24 hours of operation and 85 percent took it to within 48 hours. The mean dose of propranolol was 77 mg/day (range, 10 to 320 mg/day). Anesthetic technics and agents included enflurane, halothane, N2O-narcotic-relaxant, and spinal anesthesia. There were only three episodes of hypotension, all of which responded to a decreased depth of general anesthesia, IV fluid administration, and, in one patient, a small dose of a vasopressor. There were no intraoperative or postoperative deaths. It is concluded that if propranolol is indicated for medical control of the patient's symptoms, it need not be discontinued before surgical anesthesia.