Biomedical subjects
Publications and source records attributed to K K Teo.
Explore the source record for details and available documents.
Congestive heart failure is a potentially debilitating disorder that affects a significant number of patients. The age-adjusted death rate has doubled over the past decade. Patients live an average of 4 to 5 years, and nearly all suffer from fatigue and breathlessness, which limits exercise capacity and produces a poor quality of life. Patients have usually been advised to avoid exercise because of concerns that they would experience a further decline in cardiac function. However, it has been demonstrated that exercise capacity is not related to the degree of left ventricular systolic dysfunction. This has led to the suggestion that peripheral changes in skeletal muscle and blood supply may play a major role in determining the exercise capacity of patients with congestive heart failure. Studies have demonstrated abnormalities of skeletal muscle blood flow, metabolism and structure, all of which are consistent with the impaired performance observed in these patients. Although the effects of exercise training have been examined in only a relatively few number of patients, the results have been promising. Exercise training has been found to improve exercise capacity and reduce symptoms. However, to our knowledge no data exist as to the impact of exercise training on left ventricular function, hospital stay or mortality in this population. Even though the early results are promising, they require confirmation of feasibility, clinical benefit and safety in larger, long-term randomized trials. It should be determined whether training has a long-term beneficial impact on measures more closely related to daily activities and quality of life. Ultimately, it would be important to determine whether training has an impact on mortality and morbidity.
Knowledge gained from epidemiological studies and clinical trials on hypertension has led to impressive reductions in morbidity and mortality, particularly from stroke and coronary heart disease (CHD) as complications of end-organ damage from untreated, prolonged systemic hypertension. Data on reductions in stroke when hypertension is treated have been clear and convincing from individual clinical trials. Most of these trials, however, have consistently shown only trends towards a reduction in CHD, and few have individually reported statistically significant reductions. A recent meta-analysis, however, suggests that a significant beneficial reduction in CHD exists when the overall data are examined, although at a lower magnitude of benefit and lesser degree of certainty than for stroke. The presence of left ventricular hypertrophy (LVH) increases the risk of subsequent cardiovascular disease events, cardiovascular mortality and all-cause mortality in hypertensive patients. Although echocardiography appears more sensitive than electrocardiography in diagnosing LVH, much of the information demonstrating risks from LVH is from electrocardiography data, and it is not clear how echocardiography will change the risk prediction. Some data from large clinical trials and populations studies suggest that LVH regresses, particularly if the hypertension is adequately treated. A meta-analysis of a large number of small clinical studies in hypertensive patients suggests that the 4 commonly used antihypertensive drug classes, beta-blockers, diuretics, calcium channel antagonists and ACE inhibitors, are all associated with significant reductions in left ventricular mass. While the primary indication for treatment is clearly the hypertension and not the LVH, the presence of the latter necessitates careful treatment and follow-up of these hypertensive individuals.
The effect of late percutaneous transluminal coronary angioplasty (PTCA) of an occluded infarct-related artery on left ventricular ejection fraction was studied in patients with a recent, first Q-wave myocardial infarction in a prospective, randomized study. Forty-four patients (31 men and 13 women, mean age 58 +/- 12 years) with an occluded infarct-related coronary artery were randomized to PTCA (n = 25) or no PTCA (n = 19). Patients received acetylsalicylic acid, a beta blocker and an angiotensin-converting enzyme inhibitor unless contraindicated. Left ventricular ejection fraction was determined at baseline and 4 months. Coronary angiography was repeated at 4 months. Baseline ejection fraction measured 20 +/- 12 days after myocardial infarction was 45 +/- 12% in both groups. PTCA was performed 21 +/- 13 days after the event. The primary PTCA success rate was 72%. One patient in each group died before angiographic follow-up, which was completed in 37 of the remaining 42 patients (88%; 21 with and 16 without PTCA). At 4 months, the infarct-related artery was patent in 43% of PTCA patients and in 19% of no PTCA patients (p = NS). Reocclusion occurred in 40% of patients after successful PTCA. Secondary analyses showed that the change in left ventricular ejection fraction was significantly greater in patients with a patent infarct-related artery (+9.4 +/- 6.2%) than in those with an occluded artery (+1.6 +/- 8.8%; p = 0.0096). Baseline ejection fraction also independently predicted improvement in left ventricular ejection fraction (p = 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
Explore the source record for details and available documents.
OBJECTIVE: To define contemporary age- and sex-related mortality risks and patterns of medical practice in acute myocardial infarction (AMI). DESIGN: Retrospective comparison of demographic and clinical variables, including the use of proven effective AMI medical therapy, among AMI patients cohorts from 1987 to 1992. PATIENTS/SETTING: Of a total of 2,070 AMI patients, 629 were women and 1,441, men; 951 patients were managed in university hospitals, 641 in a regional hospital, and 478 in community hospitals. INTERVENTIONS: No direct study interventions; results of practice patterns and risk analyses of the earlier (1987-90) AMI cohorts, however, were published concurrently with the actual practices of the more recent (1991-92) cohorts and may have had some indirect effect on the recent practice patterns. RESULTS: Univariate analysis showed that mortality was higher (p < 0.0001) and use of thrombolysis, beta blockers, and acetylsalicylic acid was lower (p < 0.0001) in patients 70 years of age and older, compared with younger patients, and in women, compared with men. Multivariate analysis of the entire patient sample revealed age of 75 years or older (154 percent) and age 70 to 74 years (141 percent) to be associated with the highest relative risk of death in hospital. The increased relative risk associated with previous AMI was 45 percent. Acetylsalicylic acid use was associated with the greatest decrease in relative risk of death (-69 percent), followed by beta blockers (-36 percent) and thrombolysis (-31 percent). These patterns of relative risk were the same for men and women. CONCLUSIONS: Among contemporary AMI patients, advanced age and female sex are associated with relative under-utilization of proven effective medical therapy and increased risk of dying in the hospital. Although the contribution of age to AMI risk appears greater than that of gender, survival in any high risk group would likely be improved by increased use of proven medical therapy.
Explore the source record for details and available documents.
The types of cardiac rhythm in patients with sudden death may vary considerably, depending on the underlying cardiac disease. Although ventricular tachyarrhythmias are likely to be the most common causes, a significant proportion of patients may die suddenly due to asystole, electromechanical dissociation, or cardiac rupture. Therefore, the approaches to preventing sudden death may have to be multifactorial. The classic approach of arrhythmia suppression by empiric antiarrhythmic drugs has not resulted in a decrease in sudden death mortality. Although beta blockers have only a modest effect in suppressing arrhythmias, they have been clearly proven to prevent sudden death. Other promising approaches that require further evaluation include modulation of the autonomic balance between the sympathetic and parasympathetic nervous systems (perhaps by beta blockers, exercise training, or low-dose atropine or scopolamine), relief of ischemia by medical or surgical therapy, magnesium supplementation, and mechanical devices, such as the implantable defibrillator.
OBJECTIVE: To investigate the effects of prophylactic therapy with antiarrhythmic agents on mortality in patients with myocardial infarction. DATA SOURCES AND STUDY SELECTION: Data were obtained from all completed, published or unpublished, randomized, parallel controlled trials of antiarrhythmic agents, regardless of sample size. Investigators were contacted for data on patients excluded after randomization. DATA EXTRACTION: Data on mortality were extracted by one author and confirmed where necessary by the others. DATA SYNTHESIS: Mortality data from 138 trials on 98,000 patients were combined by the Yusuf-Peto adaptation of the Mantel-Haenszel method. There were 660 deaths among 11,712 patients allocated to receive class I agents and 571 deaths among 11,517 corresponding control patients (51 trials: odds ratio [OR], 1.14; 95% confidence interval [CI], 1.01 to 1.28; P = .03). Of 26,973 patients allocated to receive beta-blockers (class II agents), 1464 died compared with 1727 deaths among 26,295 control patients (55 trials: OR, 0.81; 95% CI, 0.75 to 0.87; P = .00001). Of 778 patients allocated to receive amiodarone (a class III agent), 77 died compared with 101 deaths in 779 control patients (eight trials: OR, 0.71; 95% CI, 0.51 to 0.97; P = .03). There were 982 deaths in 10,154 patients allocated to receive a class IV agent (calcium channel blockers) and 949 deaths in 10,188 control patients (24 trials: OR, 1.04; 95% CI, 0.95 to 1.14; P = .41). CONCLUSIONS: The routine use of class I antiarrhythmic agents after myocardial infarction is associated with increased mortality. beta-Blockers have been conclusively demonstrated to reduce mortality. The limited data on amiodarone appear promising. Data on calcium channel blockers remain unpromising.
The changes in stroke volume (SV) during upright exercise were studied in 20 insulin-dependent diabetics (IDDM) and 20 age- and sex-matched controls. None of the diabetics had any cardiovascular symptoms. In addition, tests of autonomic function were conducted in the diabetics, assessing changes in heart rate (HR) during deep breathing and the Valsalva maneuver. During exercise the SV in the controls gradually increased and then remained essentially unchanged until maximum HR was achieved. Seven of the diabetics failed to sustain an initial increase in SV (fall > 15%), eight showed a "delayed" increase in SV, and the remaining five demonstrated an increasing SV over the range from rest to peak exercise. Abnormal autonomic function results were found during deep breathing (four diabetics) and the Valsalva maneuver (four diabetics). Findings indicate that cardiac function could be abnormal in IDDM without evidence of autonomic dysfunction. This abnormality could be due to a specific cardiomyopathy.
OBJECTIVE: This study reviews the short and long term outcomes of patients who underwent isolated mitral valve replacement at the University of Alberta Hospitals during the past decade. DESIGN: Data were obtained retrospectively by review of patients' hospital charts, cardiologists' follow-up charts, contact with patients' physicians, and direct telephone or mail contact with patients and/or their surviving relatives. RESULTS: The clinical outcomes of 198 consecutive patients (124 women and 74 men) who underwent isolated mitral valve replacement from January 1981 to December 1990 at the University of Alberta Hospital were reviewed. Overall early operative mortality was 11%. Deaths were mainly related to pump failure and previous mitral valve replacement. Late mortality was 17%. Follow-up data were available except in five patients. Average follow-up was 6.3 years. Overall cumulative survival was 72.9 +/- 3.4% at five years and 63.1 +/- 4.8% at 10 years. The cumulative freedom from complications was 64.3 +/- 3.9% and 36.4 +/- 4.9% at five and 10 years, respectively. Long term survival rates obtained after isolated mitral valve replacement are higher than those reported in series of medically treated patients with mitral valve disease. CONCLUSIONS: Mitral valve replacement can prolong survival as well as improve symptoms in patients with symptomatic mitral valve disease.
Cardiac denervation may affect cardiovascular responses during exercise in patients after orthotopic cardiac transplantation. In 17 such patients, haemodynamic responses and left ventricular function were examined by radionuclide ventriculography during and after supine exercise, at an average of 17.1 +/- 2.6 months after surgery. Data were also obtained during 'volume loading' brought about by leg elevation before exercise. Results were compared with those of six normal controls. At rest, heart rate was significantly faster among transplant patients than among controls (P less than 0.0003). No significant inter-group differences in changes in cardiovascular parameters were found between the two groups during leg elevation. During exercise, heart rate in transplant patients rose at a significantly slower rate than controls (P = 0.0001), but similar increases in ejection fraction, stroke volume and cardiac output were observed among transplant patients and controls. Decline in heart rate (P = 0.0001), ejection fraction (P = 0.0007) and cardiac output (P = 0.0001) was significantly slower in transplant patients during recovery. Although there were differences in rates of increases in heart rate between transplant patients and controls during supine exercise, there were no inter-group differences in increases in cardiac output and ejection fraction and changes in haemodynamic responses and left ventricular volumes.
Explore the source record for details and available documents.
This study was undertaken to determine the blood pressure (BP) and cardiac output (Qc) responses to maximal isokinetic exercise. The subjects (n = 5) performed unilateral knee extension/flexion exercise (knee exercise) and unilateral elbow extension/flexion exercise (elbow exercise) at 0.52, 1.57, and 2.62 rads.sec-1. The BP was monitored using a cannula placed in the radial artery. Heart rate (HR), stroke volume (SV), and Qc were measured by impedance cardiography. In response to isokinetic exercise, HR and Qc increased significantly (p less than .01), while the SV did not. The BP response was characterized by significant increases in systolic, diastolic, and mean arterial pressure (MAP) (p less than .01). The Qc and MAP, responses were not influenced by the exercise velocity. The adjustments in HR, MAP, and rate pressure product (RPP) to the elbow exercise were qualitatively similar to those seen during the knee exercise, but the absolute values achieved were smaller (p less than .05). Compared with maximal dynamic exercise, the HR and SV responses to the knee exercises were lower. The MAP response to isokinetic exercise equaled the highest value achieved during dynamic exercise. Findings from the present study suggest that the cardiovascular stress (the increase in HR, MAP, and RPP) associated with isokinetic exercise is independent of the velocity of movement and is proportional to the active muscle mass.
OBJECTIVE: To investigate the effect of intravenous magnesium on mortality in suspected acute myocardial infarction. DESIGN: Systematic overview of all available randomised trials in which patients were allocated to receive either intravenous magnesium or otherwise similar treatment without magnesium. SETTING: Coronary care units of several hospitals. PATIENTS: 1301 patients in seven randomised trials. MAIN OUTCOME MEASURE: Short term mortality. RESULTS: Considering the seven trials collectively there were 25 (3.8%) deaths among 657 patients allocated to receive magnesium and 53 (8.2%) deaths among 644 patients allocated control, generally during hospital follow up. This represents a 55% reduction in the odds of death (p less than 0.001) with 95% confidence intervals ranging from about one third to about two thirds. 70 of 648 patients allocated magnesium compared with 109 of 641 controls had serious ventricular arrhythmias, suggesting that magnesium reduces the incidence, though the definition varied among trials. Other adverse effects were rare in the limited number of patients for whom this data were available. CONCLUSION: Despite the limited number of patients randomised this overview suggests that intravenous magnesium therapy may reduce mortality in patients with acute myocardial infarction. Further large scale trials to confirm (or refute) these findings are desirable.
Studies of Left Ventricular Dysfunction (SOLVD) is a randomized trial of enalapril versus placebo in reducing mortality in patients with cardiac dysfunction (defined as left ventricular ejection fraction less than or equal to 35%). Before randomization, patients at risk for hypotension were hospitalized for a test dose of 2.5 mg of enalapril administered orally at baseline and again 12 hours later. As of February 1989, 89 of 7,539 (1.2%) patients had been studied during hospitalization. Baseline systolic and diastolic blood pressures were 115 +/- 18 and 73 +/- 10 mm Hg, respectively. After enalapril, systolic blood pressure decreased slightly but significantly 8 to 20 hours after the initial dose (mean reduction 8 to 11 mm Hg). In this highly selected group of 89 patients, symptoms relating to decrease in blood pressure were noted in 13 (15%). It is emphasized that most patients with cardiac dysfunction readily tolerate enalapril. However, the agent should be administered with caution to patients with advanced congestive failure and diminished baseline blood pressure, owing to a significant incidence of symptomatic hypotension.
To further evaluate contemporary risk and practice patterns in acute myocardial infarction (AMI), 402 consecutive patients with AMI between July 1, 1988, and June 30, 1989 were studied. The clinical investigations, medical therapy and outcome of patients aged greater than or equal to 70 years (n = 132; group 1) were compared with patients aged less than 70 years (n = 270; group 2). In group 1, 20% of patients had no typical cardiac pain versus 6% in group 2 (p less than 0.01). History of previous AMI, Q-wave AMI and peak creatine kinase were not different in the 2 groups. In-hospital mortality was markedly higher in group 1 (27%) than in group 2 (8%), p less than 0.01. Multivariate analysis revealed previous AMI, presentation without typical pain and age greater than or equal to 70 years to be independently associated with the greatest relative risk. Post-AMI exercise testing, ejection fraction calculations and coronary angiography were all performed less often (p less than 0.01); proven effective medical therapies, including thrombolysis, beta blockers, acetylsalicylic acid and nitrates were all used less frequently (p less than 0.01). The very high mortality and less aggressive management of elderly patients with AMI confirm similar data from our 1987 AMI patient cohort and other recently reported AMI patient outcome analyses. However, it remains uncertain why older patients with AMI are investigated and treated differently from younger patients. Further studies are warranted.
We examined the effect of high-frequency oscillatory ventilation (HFOV) on tracheal smooth muscle tension and upper airway resistance in anesthetized dogs. The animals were ventilated via a low tracheostomy by HFOV or conventional intermittent positive pressure ventilation (IPPV) with and without added positive end-expiratory pressure (PEEP). The transverse muscle tension of the trachea above the tracheostomy was measured and found to be lower during HFOV when compared with IPPV or IPPV with PEEP. When both vagi were cooled to 8 degrees C to interrupt afferent traffic from the lungs, there was no longer any difference between the modes of ventilation. In a second series of experiments, the airflow resistance of the upper airway above the tracheostomy was measured (Ruaw). During HFOV, Ruaw was significantly lower than during either IPPV or IPPV with PEEP. We conclude that HFOV induces a relaxation of tracheal smooth muscle and a reduction of upper airway resistance through a vagally mediated mechanism.