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PubMedDate not supplied

Number needed to treat in cardiac rehabilitation.

Clinicians, patients, and health policy-makers must judge whether healthcare interventions are worth the side effects, inconvenience, and costs. The number needed to treat (NNT) provides an estimate of the number of patients who need to be treated to attain an additional favorable outcome, or to prevent an additional adverse outcome, and is the reciprocal of the absolute risk reduction. The closer the NNT is to 1.0-meaning that every patient who is treated achieves a benefit-the more effective the treatment. Traditionally, mortality has been considered a primary outcome measure of the effectiveness of cardiac rehabilitation and, if the event rates in two groups (ie, rehabilitation and usual care) are known, the absolute risk reduction can be calculated and the NNT estimated. Mortality data were derived from three meta-analyses of cardiac rehabilitation trials: one published in 1988 (n = 3614), one in 1989 (n = 4247), and one in 2001 (n = 7683). The respective estimated NNT for mortality in the meta-analyses were 32, 46, and 72 (95% confidence intervals [95% CI] 19, 1403). Improved exercise tolerance and patient-perceived health-related quality of life (HRQL) are also considered important and attainable outcomes of cardiac rehabilitation but are continuous, not dichotomous, variables. If the minimal important difference for a continuous outcome is known, then the proportions of patients who improve, remain the same, or deteriorate can be determined and the NNT estimated. Exercise tolerance and HRQL data from two randomized controlled trials of 8 weeks of rehabilitation after myocardial infarction, the Cardiac Rehabilitation in Advanced Age trial (CR-AGE; n = 270) and the McMaster Early Rehabilitation Study (MERS; n = 201) were used to estimate the NNT. In CR-AGE, the improvement in exercise tolerance was significantly greater in the rehabilitation than usual care group and the estimated NNT was 5 (95% CI 3, 13). The generic global HRQL score increased significantly in CR-AGE with rehabilitation with an estimated NNT of 12 (95% CI 5, 26) but, as the subscale group differences were not significant, the NNT was not estimated. The NNT for exercise tolerance was not estimated in MERS, as the group difference was not significant. On the other hand, specific HRQL scores in MERS increased significantly with rehabilitation giving an estimated NNT for global HRQL of 6 (95% CI 3, 21) and 6 to 10 for the HRQL sub-scales. The data and the estimated NNT from the meta-analyses of cardiac rehabilitation in large numbers of patients suggest a limited mortality effect, probably reflecting current cardiology practice. The estimated NNT from the two trials with relatively small numbers of patients suggest inconsistent exercise tolerance effects and a relatively short duration for improved HRQL. Along with the classic reporting scales, information about clinical and laboratory variables, and patient preferences, the NNT is a useful additional measure of effectiveness that provides both clinicians and patients with information about the impact of cardiac rehabilitation as secondary prevention therapy.

Exercise Tolerance↗
PubMed2003

Why do older adults decide they are having difficulty with a task?

OBJECTIVE: Previous studies have identified risk factors for decline in physical function, but they have not examined specific reasons older adults report difficulty with mobility tasks. DESIGN: Community-dwelling people ( n = 160) aged 59 yr and older in an observational cohort study were questioned to determine the most common cited reasons for self-reported difficulty in task performance. RESULTS: Mobility tasks were most often reported to be difficult (66%). The reasons cited for difficulty in low exercise tolerance tasks were task modification by method (33%) and rate (33%). For high exercise tolerance tasks, reasons cited included having to modify the rate of performing the task (20%) or the method (13%). Among those who reported difficulty with low exercise tolerance mobility tasks, >80% reported modification (odds ratio, 46.4 [95% confidence limits: 9.75, 220.51]) and 32% also report frequency change (odds ratio, 5.9 [95% confidence limits: 2.72, 12.85]) as the reason for perceiving difficulty. For those who reported difficulty performing high exercise tolerance-demanding tasks, >90% reported modification (odds ratio, 5.5 [95% confidence limits: 2.05, 14.88]) and 61% also report frequency changes (odds ratio, 3.9 [95% confidence limits: 1.93, 8.04]). CONCLUSION: The findings suggest that people are able to cite specific reasons for difficulty with mobility task performance, most commonly related to task modification.

Activities of Daily Living↗
PubMed1998

Perception of fatigue and quality of life in patients with COPD.

INTRODUCTION: Although dyspnea is considered the primary activity-limiting symptom in patients with COPD, other symptoms, such as fatigue, are frequently reported. The purpose of this study was to determine the relationship between fatigue and pulmonary function, exercise tolerance, depression, and quality of life in patients with COPD. METHODS: Forty-one patients (age = 62+/-8 years; FEV1 = 1.08+/-0.55 L; FEV1 percent predicted = 35.8+/-17%) from two sites participated in the study. Spirometric measures of pulmonary function were carried out in each patient. The Multidimensional Fatigue Inventory was used to measure five subscales of fatigue: general, physical and mental fatigue, reduction in activity, and reduction in motivation. The St. George Respiratory Questionnaire, used to measure quality of life, has three subscale dimensions (symptom, activity, and impact), as well as an overall or total quality of life score. Depression was measured with the Centers of Epidemiological Studies Depression Scale. In 19 patients, exercise tolerance was determined with the 6-min walking distance. RESULTS: General fatigue correlated with FEV1, percent predicted (r = -0.32, p < 0.05), exercise tolerance (r = -0.55, p < 0.05), depression (r = 0.44, p < 0.01), and overall quality of life (r = 0.75, p < 0.01). Among the dimensions of fatigue, depression correlated with general and mental fatigue only. Physical dimensions of fatigue correlated with an increase in the severity of pulmonary impairment and reduction in exercise tolerance. The cognitive components of fatigue, such as reduction in motivation and mental fatigue, were not found to be highly correlated with physical dimensions of quality of life. All five subscales of fatigue showed relationship to the functional impact dimension and total impairment score in quality of life. CONCLUSIONS: These data show a relationship between dimensions of fatigue and pulmonary function, exercise tolerance, and quality of life in COPD. Based on these results, fatigue is an important symptom requiring evaluation and management in patients with COPD. These data clarified also the relationship between depression and fatigue in this patient population.

Exercise Tolerance↗
PubMed1997

Association between the anaerobic threshold and the break-point in the double product/work rate relationship.

A break point in the double product versus work rate relationship (DPBP) during incremental exercise has previously been reported. The aim of the current study was to investigate the frequency and degree of inter-observer agreement with which a DPBP could be detected. We also wished to determine its relationship, if any, to the lactic acidosis threshold (LATla). Ten normal volunteers performed continuous incremental bicycle ergometer exercise under three different concentrations of inspired oxygen (FiO2 = 0.21, 0.15 and 0.12). In addition, a group of patients with diseases expected to result in impaired exercise tolerance performed exercise under room air conditions. Gas exchange was measured continuously and double product was measured at 15-s intervals throughout exercise using an automated sphygmomanometer. Four observers, unaware of subject identity and test condition, analysed a total of 39 tests. All four observers detected a DPBP in 29 cases (74%) and an LAT in 35 cases (90%). The intra-class correlation coefficient was 0.76 for the DPBP and 0.93 for the LATla, indicating a reasonable level of agreement among observers for both break points. The DPBP was closely related to the LATla (r = 0.865, P < 0.0001), although it occurred at a slightly higher oxygen consumption (VO2, bias 0.137 1.min-1, 95% confidence intervals 0.041-0.233). We conclude that the DPBP is a common occurrence during incremental exercise. The close relationship between the DPBP and the LATla suggests that both may reflect similar events at the level of the skeletal muscle cell.

Acidosis, Lactic↗
PubMed2006

Primary prevention for patients with intermediate Framingham risk scores.

Coronary heart disease (CHD) is the leading cause of mortality in the industrialized world. Proper identification of individuals at risk for CHD is challenging. The Framingham Risk Score, the most widely accepted tool for quantifying 10-year risk, fails to identify a great proportion of future CHD. Because of the health and economic consequences of CHD, there is a need to develop better prognostic tools for primary prevention. Coronary artery calcium scoring, C-reactive protein measurement, and heart rate recovery and exercise tolerance during exercise stress test may be useful tools for better risk stratification of intermediate-risk patients.

C-Reactive Protein↗
PubMed1993

The xamoterol experience in the treatment of heart failure.

Beta blockers may benefit patients with dilated cardiomyopathy but low output failure can be a problem. Thus a beta 1-selective beta blocker with about 45% intrinsic sympathomimetic activity (ISA), such as xamoterol, was thought to have a desirable pharmacologic profile. Long-term studies of xamoterol in patients with idiopathic dilated cardiomyopathy have shown improved cardiac performance and exercise tolerance, while exercise heart rate, left ventricular ejection fraction, and pulmonary artery wedge pressure were decreased. This improvement in exercise capacity and overall quality of life in patients treated with xamoterol has been confirmed in further controlled trials of patients with mild-to-moderate heart failure (NYHA class I and II). However, in patients with moderate-to-severe heart failure (NYHA class III and IV), mortality was unfavorably influenced by xamoterol. The therapeutic role of xamoterol in patients with heart disease needs further refinement.

Cardiac Output, Low↗
PubMed1987

Differences in left ventricular function between anterior and inferior myocardial infarction of equivalent enzymatic size.

The reasons for the poorer prognosis of anterior versus inferior myocardial infarction of equivalent enzymatic size remain uncertain. We investigated whether there are differences in left ventricular function between patients with anterior and inferior infarctions of equivalent enzymatic size to account for their differing outcomes. Clinical, serum enzyme, and electrocardiographic data were prospectively recorded in a consecutive series of patients less than 70 years of age with their first myocardial infarction. At 29 +/- 6 days following infarction, ejection fraction and left ventricular wall motion were assessed by gated heart scintigraphy and functional capacity by treadmill exercise testing in 19 patients with anterior and in 23 patients with inferior myocardial infarction. Peak creatine kinase and QRS scores were used to estimate total infarct size and left ventricular infarct size respectively. The anterior infarcts were of similar size to the inferior infarcts as determined by peak creatine kinase (1444 [mean] +/- 1161 [SD] U/L versus 1484 [mean] +/- 1182 [SD] U/L, respectively, P = 0.91) and peak aspartate transaminases (174 +/- 112 U/L versus 164 +/- 102 U/L, P = 0.78). The anterior myocardial infarct group had a greater percentage of the left ventricle infarcted on QRS scoring than the inferior infarct group (25.9 +/- 14.4% versus 11.1 +/- 6.0% respectively, P = 0.0004), lower global left ventricular ejection fraction (45.8 +/- 16% versus 54.6 +/- 9.2%, P = 0.04) and greater left ventricular regional wall abnormality. A significant negative correlation existed between left ventricular ejection fraction and peak creatine kinase for both groups, but was more marked with anterior infarction (r = -0.78, P less than 0.01) compared with inferior infarction (r = -0.49, P less than 0.05). Exercise-induced ST segment elevation was more frequent in the anterior than the inferior infarct group (59% versus 18%, P less than 0.02). However, both infarct locations had similar exercise tolerance, exercise-induced angina and ST segment depression. Despite equivalence of infarct size of the two infarct locations on enzyme testing, anterior infarction was associated with greater abnormality of left ventricular function with lower resting global left ventricular ejection fraction; greater resting left ventricular regional wall abnormality and greater exercise-induced ST segment elevation. These differences probably contribute to the poorer prognosis of patients with anterior infarction compared to those with inferior infarction of equivalent enzymatic size, given the previously well-documented prognostic importance of left ventricular function.

Aged↗
PubMed1997

Oral nitrates: more than symptomatic therapy in coronary artery disease?

The predominant venodilator properties of the nitrates and their augmentation of collateral coronary blood flow to the ischemic myocardium endows them with some ideal characteristics for treating myocardial ischemic syndromes. Additional efficacy stems from the ability of the nitrates to replenish the deficient endothelium-derived relaxing factor (EDRF), nitric oxide (NO), in patients with coronary heart disease and also to inhibit platelet aggregation. In stable angina pectoris, the antianginal and antiischemic effects of oral nitrates are well established. Continuous administration of nitrates may lead to tolerance of their clinical efficacy. Recent studies, however, have demonstrated that when used in recommended doses, tolerance can be avoided during long-term treatment with oral nitrates without provocation of anginal attacks during periods of low nitrate levels at night and early hours of the morning. Thus, prolonged treatment with an asymmetric twice-daily regimen of immediate-release isosorbide-5-mononitrate in patients with stable angina pectoris does not give rise to clinical tolerance, prolongs exercise duration, and delays the onset of myocardial ischemia. In unstable angina pectoris, nitrates rapidly relieve chest pain and ameliorate the electrocardiographic signs of myocardial ischemia. In patients with acute myocardial infarction, early treatment with nitrates prevents left ventricular dilatation, improves pumping function, and reduces the risk of ventricular arrhythmias. In patients with chronic heart failure, oral nitrates improve exercise tolerance and, when given in combination with the systemic arterial dilator hydralazine, extend survival. Meta-analysis of published studies has demonstrated that both intravenous and oral nitrates reduced infarct size and morbidity and mortality in patients with acute myocardial infarction. In the ISIS 4 post-infarction study, isosorbide-5-mononitrate 60 mg once daily was not superior to placebo in reducing mortality risk. However, in the GISSI 3 study, the combination of nitrates with an angiotensin-converting enzyme (ACE) inhibitor reduced mortality risks by 17% in patients with acute myocardial infarction. In both the ISIS 4 and GISSI 3 studies, 62% and 57% of the patients in the placebo and control groups, respectively, were treated with nitrates for control of rest angina, myocardial ischemia, and or left ventricular failure symptoms, and this widespread use of open-label nitrates in the control groups may have diluted the true beneficial effects of nitrates in both studies. Taken together, these many studies with oral nitrate treatment in coronary heart disease and heart failure clearly emphasize that these drugs are safe and play more than a symptomatic role in the management of patients with acute and chronic ischemic syndromes due to coronary artery disease.

Administration, Oral↗
PubMed2003

Abnormal cardiac and skeletal muscle energy metabolism in patients with type 2 diabetes.

BACKGROUND: It is well known that patients with type 2 diabetes have increased risk of cardiovascular disease, but it is not known whether they have underlying abnormalities in cardiac or skeletal muscle high-energy phosphate metabolism. METHODS AND RESULTS: We studied 21 patients with type 2 diabetes with no evidence of coronary artery disease or impaired cardiac function, as determined by echocardiography, and 15 age-, sex-, and body mass index-matched control subjects. Cardiac high-energy phosphate metabolites were measured at rest using 31P nuclear magnetic resonance spectroscopy (MRS). Skeletal muscle high-energy phosphate metabolites, intracellular pH, and oxygenation were measured using 31P MRS and near infrared spectrophotometry, respectively, before, during, and after exercise. Although their cardiac morphology, mass, and function appeared to be normal, the patients with diabetes had significantly lower phosphocreatine (PCr)/ATP ratios, at 1.50+/-0.11, than the healthy volunteers, at 2.30+/-0.12. The cardiac PCr/ATP ratios correlated negatively with the fasting plasma free fatty acid concentrations. Although skeletal muscle energetics and pH were normal at rest, PCr loss and pH decrease were significantly faster during exercise in the patients with diabetes, who had lower exercise tolerance. After exercise, PCr recovery was slower in the patients with diabetes and correlated with tissue reoxygenation times. The exercise times correlated negatively with the deoxygenation rates and the hemoglobin (Hb)A1c levels and the reoxygenation times correlated positively with the HbA1c levels. CONCLUSIONS: Type 2 diabetic patients with apparently normal cardiac function have impaired myocardial and skeletal muscle energy metabolism related to changes in circulating metabolic substrates.

Adenosine Diphosphate↗
PubMed1988

Pulmonary rehabilitation in COPD patients with elevated PCO2.

Exercise programs are a mainstay of pulmonary rehabilitation for COPD. COPD patients with elevated PCO2 are severely impaired and might benefit from rehabilitation more than other patients. However, there is no systematic data to indicate that hypercapnic COPD patients benefit from intensive rehabilitation. Indeed, in patients with hypercapnia, increased exercise might overtax respiratory muscles, which are weak relative to those of eucapnic patients. To investigate this issue, we reviewed all COPD patients admitted to our pulmonary inpatient program from 1983 to 1986 (n = 317). The program includes multiple daily sessions of upper and lower extremity exercise to tolerance. We assessed admission and discharge pulmonary function tests, arterial blood gases (room air), and functional status. Ambulation distance on a 6-min walk test was used as an objective measure of functional status. Patients were grouped according to the results of their admission room air PCO2. We found that eucapnic patients (n = 197) significantly increased ambulation (admission to discharge) from 409 to 816 feet (p less than 0.001). Hypercapnic patients improved as well. Patients with moderate hypercapnia (PCO2, 45 to 54 mm Hg; n = 86) increased their ambulation from 330 to 663 feet (p less than 0.0001). Patients with severe hypercapnia (PCO2 greater than 54 mm Hg; n = 34) increased their ambulation from 336 to 597 feet (p less than 0.0001). We found a small but significant improvement in discharge pulmonary function and arterial blood gas results. We conclude that COPD patients with hypercapnia, despite severe ventilatory impairment and weak respiratory muscles, tolerate exercise well and benefit significantly from intensive inpatient pulmonary rehabilitation.

Carbon Dioxide↗
PubMed2000

Drug interaction between cimetidine and timolol ophthalmic solution: effect on heart rate and intraocular pressure in healthy Japanese volunteers.

Systemic adverse effects of timolol ophthalmic solution given at usual therapeutic doses have been well characterized. Timolol is partially metabolized by cytochrome P450 (CYP) 2D6. Cimetidine inhibits the activity of cytochrome P450, including CYP2D6, leading to reduced systemic clearance of concomitant drugs. Coadministration of cimetidine has been speculated to affect the pharmacological effects of timolol ophthalmic solution, resulting in increased blood concentration. To evaluate whether administration of cimetidine with timolol ophthalmic solution increased the degree of beta-blockade, 12 healthy Japanese male volunteers ages 19 to 26 received cimetidine (400 mg), on oral placebo, timolol maleate 0.5% (0.05 mL to each eye), or placebo eye drops in a randomized, double-blind, Latin-square design. The oral drug alone was given for 3 days, and on the 4th day, eye drops were applied after oral drug administration. At baseline and 1, 3, and 6 hours after eye drop administration, blood pressure and heart rate (HR) were measured before and after exercise. Intraocular pressure (IOP) was measured at rest. A visual analog scale (VAS) was used to assess subjective bodily feelings in exercise tolerance after every physical exercise. The exercise HR, exercise systolic blood pressure (SBP), and resting SBP were reduced following timolol with and without cimetidine compared with the placebo (p < 0.01, respectively). Administration of cimetidine with timolol ophthalmic solution resulted in additional reductions of the resting HR and IOP. VAS detected a significant reduction in exercise tolerance from timolol ophthalmic solution (p < .05). In conclusion, administration of cimetidine with timolol ophthalmic solution increased the degree of beta-blockade.

Adrenergic beta-Antagonists↗
PubMed1997

Exercise for patients with congestive heart failure.

Congestive heart failure is a widely prevalent sequel to myocardial infarction and other chronic conditions (including ischaemia without infarction, hypertension, various infections, toxic metabolic and endocrine disorders). Exercise tolerance is severely limited; the cardiac ejection fraction is often less than 20% and the peak oxygen intake may be less than 10 ml/kg x min, with a resulting deterioration in the quality of life. Possible factors contributing to the poor tolerance of exercise include: (i) disturbances of myocardial function (damage to the ventricular wall; decreased inotropic response, mitral valve regurgitation and increased diastolic pressures); (ii) peripheral vascular factors (decreased metaboreceptor discharge, reduced vasodilator response, increased activity of sympathetic afferents and less efficient distribution of cardiac output); (iii) hormonal disturbances (increases of catecholamines, renin/angiotensin/aldosterone, antidiuretic and natriuretic factors, endothelin and decreased endothelium-relaxing factor); (iv) impaired muscle function (loss of lean tissue, increase of type II fibres, increased impedance to perfusion, enzyme changes); (v) ventilatory disturbances (increased oxygen cost of activity, pulmonary congestion, increased ventilatory drive, mismatching of ventilation and perfusion, increased anaerobic effort); and (vi) psychological factors (anxiety, depression and iatrogenic limitation of effort). The prognosis with conventional treatment is poor, but patients with stable congestive heart failure respond favourably to a progressive exercise programme. Reported gains depend on the cause of congestive failure, initial status, study duration and compliance, and the type of training programme. Most studies to date have been short term (4 to 16 weeks), and relatively few have adopted a randomised controlled design. Suggested bases for the enhancement of aerobic performance of up to 20% include an increased intensity of peak effort, an enhanced matching of ventilation to perfusion, improved cardiac function, a strengthening of skeletal muscle and an increase of aerobic enzyme activity in the muscles. A few studies have continued for a year or longer and it appears that the gains realised over the first 16 weeks of training can be sustained for this period; the quality of life is enhanced, but data are as yet insufficient to judge effects upon mortality rates. Useful clinical information can be obtained from a 6-minute walk, but the choice for more precise evaluation lies between a measurement of ventilatory threshold or peak oxygen intake. Given initial muscle wasting, prescribed exercise should include both aerobic activity and resisted muscle exercises.

Cardiovascular System↗
PubMed1979

Therapeutic effects of pindolol and nifedipine in patients with stable angina pectoris and asymptomatic resting ischemia.

A single blind randomized parallel study designed to assess the anti-anginal efficacy of pindolol and nifedipine was carried out in 42 ambulatory coronary patients with stable angina pectoris. Drug efficacy was assessed in terms of (a) pain, (b) frequency of anginal episodes, (c) nitroglycerin consumption, (d) exercise tolerance and (e) ST-segment changes. The effect of these drugs on asymptomatic resting myocardial ischemia was also assessed by means of 24-h dynamic electrocardiography (DCG). All patients were checked at weekly intervals. At the end of a 4-wk placebo period, the patients were randomly assigned either to the pindolol or nifedipine group. The treatment lasted for 45 days. During the placebo period, ischemic ECG changes and symptoms of coronary insufficiency were detected in all patients. Furthermore, 12 out of 42 patients had asymptomatic myocardial ischemia at rest. One patient from each group was dropped because of tolerance. At the end of the 45-day study, pindolol and nifedipine were equi-effective on spontaneous and effort-related angina. There were, however, some differences: increased tolerance to exercise appeared earlier with pindolol: the pindolol group showed a slightly reduced while the nifedipine group showed a slightly increased heart rate. Furthermore, nifedipine reduced or eliminated asymptomatic myocardial ischemia in 6 out of 7 patients while only 1 out of 5 improved in the pindolol group.

Adult↗
PubMed2003

[Endothelial protection in patients with apparent cardiac failure in long-term therapy by carvedilol].

We studied effects of beta-adrenoblocker carvedilol vs placebo in 60 patients with chronic cardiac failure (CCF) of functional classes III-IV in a 6-month open randomized trial. We examined clinical course, exercise tolerance (a 6 min walk test), endothelial state markers (endothelium-dependent vasodilation, number of circulating endotheliocytes) and activity of systems affecting endothelium (triglycerides, malonic dialdehyde, IL-8, uric acid). The drug was added to conventional therapy (ACE inhibitors, diuretics, cardiac glycosides) in a stable CCF course. Carvedilol group of patients demonstrated a marked trend to reduction of the number of hospitalizations, attenuation of CCF, better tolerance to exercise, lower levels of uric acid (p < 0.05), malonic dialdehyde (p < 0.05) and IL-8 (p = 0.09). There was also wider basal diameter of the brachial artery, and in the diameter at the peak of reactive hyperemia (p = 0.07). The effect was dose-dependent: in patients given 25-50 mg/day of carvedilol there was a trend to a lower circulation of endotheliocytes, triglyceridemia, lipid peroxidation and chronic inflammation. Thus, long-term treatment of CCF with inclusion of standard doses of carvedilol not only improves clinical status of the patients but produces a noticeable endothelioprotective effect.

Adrenergic beta-Antagonists↗
PubMed2004

Timing of surgery in asymptomatic aortic stenosis.

Prospective studies have convincingly shown that sudden death in asymptomatic patients with AS is rare and prognosis is good as long as LV function, exercise tolerance and exercise hemodynamics remain normal. The time interval to development of LV dysfunction is not known. Therefore the initial evaluation should be confirmed after 3-6 months including echocardiography and exercise testing to identify patients with rapid progression, LV dysfunction and other high risk patients in whom surgery can be expected to improve prognosis even if the patient remains asymptomatic.

Aortic Valve Stenosis↗
PubMed1991

The prognosis in stable and unstable angina.

The average annual mortality in unselected patients with chronic stable angina is 4%. Mortality is increased in male patients and in patients who have risk factors such as hypertension, previous MI, or abnormal ECGs. We do not routinely recommend cardiac catheterization in the initial management of patients with stable angina unless the patient exhibits evidence for severe myocardial ischemia on non-invasive testing or has symptoms that are refractory to treatment. In patients who undergo cardiac catheterization, the most important determinant of survival is left ventricular function followed by the number of diseased vessels. Noninvasive testing provides important additional prognostic information to cardiac catheterization data and should be used in the decision to treat a patient medically or surgically. Mortality is increased in patients who have low exercise tolerance, exercise-induced ischemia, or a poor hemodynamic response to exercise. Unstable angina in medically treated patients is associated with a 3% to 5% hospital mortality and 7% to 8% mortality in the first year. The rate of nonfatal MI is about 8% to 10% in the first 2 weeks. We routinely recommend coronary angiography unless patients have had recent cardiac catheterization or there is a major contraindication. Mortality is increased in those who fail to respond to initial therapy, who have severe left ventricular dysfunction, and who have multivessel CAD, particularly left main CAD. The question of whether all patients with unstable angina require coronary angiography for risk stratification and possible revascularization is being addressed in the TIMI III trial.

Adult↗
PubMed1989

Chronic effects of transdermal nitroglycerin in stable angina pectoris: a within-patient, placebo-controlled study.

The efficacy of transdermal nitroglycerin patches, releasing 20 mg of active substance over a period of 24 h (TDN 20), was investigated in 10 patients with stable exercise-induced angina pectoris. The study was divided into 3 periods: the first part was an acute, within-patient, crossover, double-blind, placebo-controlled study, in which patients performed a cycloergometric exercise test 4 and 24 h after the application of the patches (TDN 20 or placebo). During the 2nd period, patients were given TDN 20, in single blind conditions, for 4 weeks and another exercise test was performed, on the last day, 4 and 24 h after patch application. Finally, after a one-day placebo wash-out, a second acute study similar to the first was performed. Four h after dosing, exercise duration to 1 mm ST segment depression was 441 s and 314 s (p less than 0.01) for TDN 20 and placebo, respectively (first acute study), 394 s for TDN 20 after chronic treatment (p less than 0.001 vs acute placebo) and 472 and 354 s (p less than 0.001) for TDN 20 and placebo, respectively (second acute study). No difference in exercise duration to 1 mm ST segment depression was found between TDN 20 and placebo, 24 h after administration, in any of the periods. Blood pressure significantly decreased and heart rate significantly increased 4 h after TDN dosing (in comparison with placebo) in both the acute studies, but no difference was observed after chronic TDN treatment. In conclusion, TDN 20 increases exercise tolerance 4 h after the application of both acute and chronic treatments.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Cutaneous↗