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Biomedical subjects

L B Tan

Publications and source records attributed to L B Tan.

At least 37 records · Page 2Linked to original sources
PubMed1999

The role of exercise testing in the evaluation and management of heart failure.

The clinical syndrome of heart failure has been investigated so extensively that it may now almost be regarded as a metabolic disorder. Although an initial insult reduces cardiac pump efficacy, the resultant physiological response culminates in complex neurohormonal dysfunction. This has created confusion and prevented the acceptance of a universal definition of cardiac failure. With much current research concentrating on the pharmacological modification of neuroendocrine imbalance, it is easy to lose sight of the fundamental principles behind heart failure management, namely, to improve cardiac function. In attempting to achieve this, the issues of morbidity and mortality must be addressed jointly; they are not mutually exclusive entities. Discrepant results between mortality studies and changes in exercise capacity have undermined the value of exercise testing. Because a treatment enhances longevity we should not ignore its effect on symptomatic status, and likewise we should not discard a therapy, which improves function because adverse events result in occasional premature deaths. Informed patient choice must exist. Historically, exercise testing has been quintessential in our understanding and evaluation of heart failure. Peak oxygen consumption remains the best overall indicator of symptomatic status, exercise capacity, prognosis and hospitalisation. Unfortunately, muddling of surrogate and true end-points has confused many of these issues. Improved comprehension may be gained by applying the concept of cardiac reserve which has been described in a variety of heart conditions and used in cardiac failure patients to provide an indication of prognosis and functional capacity.

Exercise Test↗
PubMed1998

Physiological cardiac reserve: development of a non-invasive method and first estimates in man.

OBJECTIVE: To investigate whether physiological cardiac reserve can be measured in man without invasive procedures and whether it is a major determinant of exercise capacity. DESIGN: Development of method of measurement and an observational study. SETTING: A regional cardiothoracic centre. SUBJECTS: 70 subjects with a wide range of cardiac function, from heart failure patients to athletes. METHODS: Subjects underwent treadmill, symptom limited cardiopulmonary exercise tests to measure aerobic exercise capacity (represented by VO2max) and cardiac reserve. Cardiac output was measured non-invasively using the CO2 rebreathing technique. RESULTS: Cardiac power output (CPOmax) at peak exercise was found to be significantly related to aerobic capacity: CPOmax (W) = 0.35 + 1.5 VO2max (1/min), r = 0.87, p < 0.001. It also correlated well with exercise duration (r = 0.62, p < 0.001), suggesting that cardiac reserve is a major determinant of exercise capacity. In the study, cardiac reserve ranged from 0.27 to 5.65 W, indicating a 20-fold difference between the most impaired cardiac function and that of the fittest subject. CONCLUSIONS: A non-invasive method of estimating physiological cardiac reserve was developed. The reserve was found to be a major determinant of exercise capacity in a population of normal subjects and patients with heart disease. This method may thus be used to provide a clearer definition of the extent of cardiac impairment in patients with heart failure.

Adolescent↗
PubMed1996

Synchronous bilateral carcinoma of the ureter in association with unilateral incomplete duplication of the ureter.

A case of bilateral synchronous ureteral tumors, in association with a unilateral incomplete duplication of ureter, is presented. This patient underwent right nephroureterectomy with removal of a cuff of bladder, partial resection of left ureter, and ileal loop interposition between renal pelvis and bladder. Followup showed no recurrence in the residual urinary tract 2-years postoperatively.

Carcinoma, Transitional Cell↗
PubMed1996

Heart failure: can it be defined?

Unlike hypertension, heart failure is not readily identified, defined and evaluated. Research and clinical management of heart failure has been handicapped by the absence of a clear definition. In other branches of medicine, e.g. renal or pulmonary failure can be clearly defined with the help of direct measures of organ function. Unfortunately such a parameter does not exist in cardiology to help us with defining cardiac function or failure. Representative definitions of heart failure hitherto proposed are reviewed. A common error in these 'definitions' is the confusion between formulating a definition and giving instructions on how to identify or diagnose heart failure. Other short-comings are also recognised. From these it is possible to compile criteria which a definition of heart failure should possess. When formulating any definition, in order to avoid unnecessary detail, the importance of including only the essence and not the contingents is recognised. To find a new definition which complies best with these criteria is an important challenge facing cardiologists.

Cardiac Output↗
PubMed1996

The concept of cardioreparation: Part 1. Pathophysiology of remodelling.

PURPOSE: Left ventricular hypertrophy is common in patients with hypertension or congestive heart failure and in survivors of myocardial infarction. It is associated with increased risks of adverse cardiovascular events, including angina, myocardial infarction and congestive heart failure. We aimed to explain these observations in terms of changes in the structure of the heart, collectively described as remodelling. DATA EXTRACTION: Laboratory investigations of animal models of cardiovascular diseases were reviewed. The most prominent features of remodelling are myocyte hypertrophy, excessive accumulation of collagen in the heart (myocardial fibrosis) and pathological changes in the coronary blood vessels. Remodelling disrupts the structure of the heart and impairs its pumping function and blood supply. The reversal of remodelling, termed cardioreparation, could restore cardiac structure and function towards normal and improve the prognosis of patients with cardiovascular diseases. CONCLUSIONS: Cardioreparation implies the regression of myocyte hypertrophy and myocardial fibrosis. Myocyte hypertrophy is primarily a response to chronic pressure or volume overload of the ventricles, whereas myocardial fibrosis depends on activation of circulating and tissue renin-angiotensin-aldosterone systems. Angiotensin converting enzyme inhibitors reduce blood pressure and inhibit these systems. They might therefore induce cardioreparation.

Cardiovascular Diseases↗
PubMed1996

The concept of cardioreparation: Part 2. Medical implications of cardioreparation.

PURPOSE: Left ventricular hypertrophy (LVH) caused by systemic hypertension, myocardial infarction and congestive heart failure is associated with pathological changes in the structure of the heart, collectively described as remodelling (see part 1 of this review). The reversal of remodelling, termed cardioreparation, might restore cardiac structure and function towards normal, thereby improving the prognosis of these conditions. We aimed to explore the medical implications of this concept. DATA EXTRACTION: Clinical trials of angiotensin converting enzyme (ACE) inhibitors and other drugs in patients with hypertension, myocardial infarction and congestive heart failure were reviewed. The results showed that ACE inhibitors induce regression of LVH in hypertensive patients, reduce mortality in acute myocardial infarction, and reduce morbidity and mortality in patients with congestive heart failure or left ventricular dysfunction subsequent to myocardial infarction. These observations are consistent with cardioreparation by ACE inhibitors. CONCLUSIONS: ACE inhibitors reduce morbidity and mortality in patients with myocardial infarction or congestive heart failure. Theoretical considerations and some clinical observations suggest that these benefits might result from cardioreparation.

Antihypertensive Agents↗