Biomedical subjects
Publications and source records attributed to S D Pringle.
Percutaneous balloon dilatation of the pulmonary valve resulted in long lasting benefit in a 40-year-old patient with carcinoid heart disease. Concomitant aggressive therapy for her metastatic carcinoid tumour may explain why the clinical outcome was better than previous reports.
Transoesophageal echocardiography was used to investigate the haemodynamic profile achieved during active compression-decompression cardiopulmonary resuscitation in humans. The mechanism of antegrade blood flow achieved by ACD-CPR is consistent with the cardiac pump theory. Improved right heart compression, antegrade blood flow patterns and left ventricular filling were observed in some patients during ACD-CPR.
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In view of the increased risk of cardiac events in systemic hypertension, particularly in patients with left ventricular hypertrophy, it is important to have reliable methods of assessing cardiac structure and function and myocardial perfusion in these patients. While echocardiography is the noninvasive method of choice for measuring the severity of left ventricular hypertrophy there is no alternative at present to invasive coronary angiography to define accurately coronary artery anatomy. Nuclear cardiological investigations are extremely useful in the assessment of systolic and diastolic function at rest and during exercise. Furthermore, myocardial perfusion imaging is of value in identifying myocardial ischaemia and assessing the functional importance of coronary artery lesions. Recent studies have also suggested that nuclear cardiology investigations may be the best way to identify nonfunctioning but viable areas of the myocardium which may benefit from revascularization.
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OBJECTIVE: To evaluate the relationship between sudden cardiac death, ventricular arrhythmias and left ventricular hypertrophy in patients with hypertension. DATA IDENTIFICATION: Epidemiological studies assessing the importance of left ventricular hypertrophy as a risk factor for sudden cardiac death, studies assessing the prevalence of arrhythmias in left ventricular hypertrophy and studies assessing whether there is an electrophysiological substrate in the hypertrophied myocardium for ventricular dysrhythmias. RESULTS OF DATA ANALYSIS: Current evidence indicates that left ventricular hypertrophy is a risk factor for sudden cardiac death and that ventricular arrhythmias are more prevalent in hypertensive patients with than in those without left ventricular hypertrophy. However, there is a lack of evidence that these dysrhythmias are important as an underlying mechanism for sudden cardiac death, and there is no clear evidence that the hypertrophied myocardium is, itself, an arrhythmogenic substrate for malignant ventricular dysrhythmias. One possible mechanism for sudden cardiac death is myocardial ischaemia, either as a consequence of associated coronary disease or due to left ventricular hypertrophy, but this remains unproved. CONCLUSIONS: There is currently no evidence that the ventricular ectopic activity seen in patients with hypertensive left ventricular hypertrophy is a marker for sudden cardiac death. Clarification of the mechanisms involved in sudden cardiac death will help in selecting appropriate preventive and therapeutic strategies for these patients.
The antihypertensive, biochemical and adverse effects of captopril, hydralazine, nifedipine and placebo were compared in 160 patients with BP inadequately controlled by atenolol 100 mg daily plus bendrofluazide 5 mg daily. Treatments were given for up to 12 weeks. Beta-blocker and thiazide were continued unchanged. All three active drugs reduced supine BP relative to placebo; mean BP changes attributable to active treatment (95% confidence intervals): captopril 13.4/10.3 mmHg (0.6/4.0 to 26.2/16.6), hydralazine 15.0/10.0 mmHg (1.7/3.4 to 28.3/16.6), nifedipine 16.8/8.1 mmHg (4.0/1.8 to 29.6/14.4). There were no significant differences between the agents. Results for erect BP were similar. Target BP (< 140/95 mmHg) was achieved more frequently on captopril (33%), hydralazine (29%) and nifedipine (17%) than on placebo (10%). Compared with the other treatments captopril increased serum potassium concentration (P = 0.01), and hydralazine reduced serum cholesterol concentration (median changes: captopril -0.2 mmol/l, hydralazine -0.8 mmol/l, nifedipine -0.2 mmol/l, and placebo +0.2 mmol/l, P < 0.001). Overall, side-effects did not differ significantly between the groups; withdrawals resulting from adverse reactions: captopril 15%, hydralazine 24%, nifedipine 22%, and placebo 3% (chi 2 = 8.2, P = 0.04). Captopril, hydralazine and nifedipine did not differ significantly in efficacy and tolerability when added to atenolol and bendrofluazide. However, there were trends in favour of captopril, on which drug the highest proportion of patients had their BP controlled and the lowest proportion were withdrawn because of side-effects. Thus, of the drugs tested, captopril appears to be the best option as third drug in hypertension.
The objective of this study was to examine the contribution of beta-blockade to antihypertensive treatment regimens including an angiotensin converting enzyme inhibitor or a calcium antagonist. The effects on BP control, adverse events, and plasma active renin concentration of removing atenolol from standard triple therapy (bendrofluazide and atenolol together with captopril or nifedipine) were assessed in a double-blind, randomised, parallel-group study, of eight weeks' duration in 46 patients from the Glasgow Blood Pressure Clinic. Blood pressures rose in patients randomised to placebo-atenolol compared with those who continued active-atenolol although the difference did not achieve statistical significance. However, the proportion of patients with controlled blood pressure (supine systolic BP < 140 mmHg plus supine diastolic BP < 95 mmHg) fell from 31% to 0% over the study period in patients given placebo-atenolol. There was a trend for BP control to deteriorate most when atenolol was withdrawn from nifedipine treated patients, but the 95% confidence intervals for the difference from captopril-treated patients were wide. Few side-effects were seen and these did not differ quantitatively between the study groups. Plasma active renin concentration was initially higher in captopril-treated patients, and increased on withdrawal of atenolol in both groups. Our findings suggest that beta-blockers make a clinically relevant contribution to treatment regimens including angiotensin converting enzyme inhibitors or calcium antagonists when given as part of standard triple antihypertensive therapy.
M-mode echocardiograms of 202 cardiac patients were studied with respect to the pattern of left ventricular (LV) geometry. Patients with normal LV mass and volume were separated from those who had LV hypertrophy or enlargement on the basis of LV mass and volume indexed to body surface area. The relative wall thickness that is currently used to classify LV hypertrophy/enlargement was found to be inadequate for differentiating between concentric and eccentric types of LV hypertrophy. A new M-mode echocardiographic classification is therefore proposed that accurately separates the different types of LV enlargement; it also allows identification of patients who have chronically dilated left ventricles at the expense of thin walls and thus have normal LV mass.
Hypertensive patients with the electrocardiographic (ECG) pattern of left ventricular (LV) hypertrophy and strain are at increased risk of sudden death. It has been suggested that ventricular arrhythmias may be responsible. The prevalence and significance of ventricular arrhythmias was therefore studied in 90 hypertensive patients with LV hypertrophy and strain by undertaking 48-hour ambulatory ECG monitoring, ECG signal-averaging and programmed ventricular stimulation. Complex ventricular ectopic activity (Lown grade greater than or equal to 3) was detected in 59 patients (66%). Eleven patients (12%) had episodes of nonsustained ventricular tachycardia. There were no sustained arrhythmias either on ambulatory ECG monitoring or induced by programmed ventricular stimulation. Only 1 patient had ventricular late potentials recorded by the signal-averaged electrocardiogram. Therefore, there was little to suggest an underlying arrhythmogenic substrate in these patients. In conclusion, whereas ventricular arrhythmias occur often in patients with LV hypertrophy associated with systemic hypertension, their significance, if any, remains to be established.
BACKGROUND: Classically, the ST-T configuration in the electrocardiogram of patients with left ventricular hypertrophy is said to have a typical pattern of ST depression together with asymmetrical T wave inversion (the so-called left ventricular strain pattern). However, many patients with left ventricular hypertrophy may also have ischaemic heart disease. To revise the electrocardiographic criteria for left ventricular hypertrophy the ST-T configuration in patients with left ventricular hypertrophy documented by echocardiography and with normal coronary arteries was assessed. METHODS: 24 patients were selected for this study. All had left ventricular hypertrophy documented by echocardiography, normal coronary arteries by cardiac catheterisation, and ST and/or T wave abnormalities in the lateral leads of their electrocardiogram. There were eight patients with aortic valve disease and 16 with hypertension who had coronary angiography as part of an investigation into the risk factors of sudden cardiac death caused by hypertensive left ventricular hypertrophy. No patient was receiving digitalis preparations or had electrolyte disturbances, and none had a previous myocardial infarction or ventricular conduction defect. RESULTS: Typical electrocardiographic evidence of left ventricular strain was found in approximately two thirds (63%) of patients and 95% of this subgroup had asymmetrical T wave inversion. Flat ST segment depression, with or without T wave inversion or isolated T wave inversion (symmetrical or asymmetrical) in the anterolateral leads, was seen in the remaining 37% of patients. CONCLUSIONS: These findings indicate that left ventricular hypertrophy without coronary artery disease can cause variable types of ST-T abnormalities in the anterolateral leads including the typical left ventricular strain pattern and non-specific ST-T changes. Non-specific abnormalities could not be distinguished from those of coronary artery disease and may adversely affect the accuracy of the electrocardiographic criteria for the diagnosis of left ventricular hypertrophy because they do not accord with the criteria for left ventricular strain.
OBJECTIVE: To assess the prevalence of symptomatic and silent myocardial ischaemia in patients with hypertensive left ventricular hypertrophy. DESIGN: Cross sectional study. SETTING: University department of medical cardiology. PATIENTS: 90 patients (68 men and 22 women; mean age 57 (range 25 to 79)) with left ventricular hypertrophy due to essential hypertension. INTERVENTIONS: 48 hour ambulatory ST segment monitoring (all patients), exercise electrocardiography (n = 79), stress thallium scintigraphy (n = 80), coronary arteriography (n = 35). RESULTS: 43 patients had at least one episode of ST segment depression on ambulatory electrocardiographic monitoring. The median number of episodes was 16 (range 1 to 84) with a median duration of 8.6 (range 2 to 17) min. Over 90% of these episodes were clinically silent. 26 patients had positive exercise electrocardiography and 48 patients had reversible thallium perfusion defects despite chest pain during exercise in only five patients. 18 of the 35 patients who had coronary arteriography had important coronary artery disease. Seven of these patients gave no history of chest pain. CONCLUSIONS: Symptomatic and silent myocardial ischaemia are common in hypertensive patients with left ventricular hypertrophy, even in the absence of epicardial coronary artery disease.
To determine electrocardiographic changes and whether myocardial ischemia occurs during cesarean section, electrocardiograms were recorded continuously using Holter monitoring in 25 patients undergoing elective cesarean section under either spinal or epidural anesthesia. In addition, in 13 of the patients, two-dimensional precordial echocardiography was carried out before and during cesarean section. ST segment depression suggestive of myocardial ischemia occurred in 16 patients including 8 of the 13 with echocardiograms. Wall motion remained entirely normal during episodes of ST segment depression. Patients in whom ST depression developed had significantly more rapid heart rates at delivery than those who did not experience ST depression. We conclude that ST segment depression is a common feature of the electrocardiogram during cesarean section under regional anesthesia and is not the result of myocardial ischemia.
The Doppler echocardiographic indexes of the tricuspid and mitral valves were assessed in 74 normal subjects (35 women and 39 men, mean age 45 years). A reproducibility study was also performed to examine the various sources of technical and biological variability. There were significantly higher peak early and late flow velocities across the mitral valve than across the tricuspid valve (0.67 +/- 0.13 and 0.47 +/- 0.12 vs 0.51 +/- 0.08 and 0.35 +/- 0.09 m.s-1, respectively; all p less than 0.0001). There was no significant difference between the early:late (E:A) velocity ratios of the 2 valves (1.65 +/- 0.73 vs 1.75 +/- 0.67, p less than 0.01). There was a steeper mitral early deceleration slope (-3.59 +/- 1.07 vs -2.95 +/- 0.91 m.s-2) but no significant difference in pressure half-times across the 2 valves (47 +/- 7 vs 51 +/- 12 ms, p less than 0.1). No influence of gender or body surface area could be demonstrated. There was a weak but significant relation between mitral peak early, peak atrial velocity and E:A ratio and age (r = -0.39, p less than 0.001, r = 0.23, p less than 0.01, and r = -0.245, p less than 0.01, respectively). There was no significant correlation between any of the tricuspid flow parameters and age. Respiration caused pronounced variability in the tricuspid Doppler indexes and all tricuspid flows were sampled and analyzed only during inspiration. The intra- and interobserver variabilities were small for all of the Doppler indexes measured, but the day-to-day variability was quite significant especially for the pressure half-time, deceleration and acceleration slope values.(ABSTRACT TRUNCATED AT 250 WORDS)
We present a detailed Doppler evaluation of a left atrial myxoma. Doppler recordings varied considerably with the position of the patient and of the sample volume. Maximum obstruction to flow was observed in the left lateral position; but no gradient was present when sitting upright. These findings provide a haemodynamic explanation for the positional variation of murmurs characteristic of atrial myxomas.
Left ventricular dimensions were measured on M-mode echocardiograms, both by the Penn Convention and the Recommendations of the American Society of Echocardiographers in a sample cardiac population. The measurements of interventricular septum and the posterior wall of the left ventricle were significantly larger (P less than 0.001) using American Society Recommendations compared to using the Penn Convention. However, the left ventricular internal dimension at end-diastole was significantly larger (P less than 0.001) when measured by the Penn Convention. As a result of the differences in left ventricular dimensions, the left ventricular mass indexed to body surface area was significantly higher (P less than 0.001) using American Society as opposed to Penn measurements. On the other hand, left ventricular volume indexed to body surface area was significantly higher (P less than 0.001) on Penn measurements than on American Society estimates. These differences should be considered in any study where criteria of normality are to be applied. Good positive correlation (r greater than 0.9) between Penn and American Society estimates of indexed left ventricular volume allowed development of a regression equation to convert volumes from one convention to another. As a result, an upper normal limit of 100 ml/m2 for indexed left ventricular volume is suggested for measurements made using the Penn Convention.
Hypertension is an established risk factor for all the clinical sequelae of coronary artery disease. Despite this, individual therapeutic trials of antihypertensive therapy have not demonstrated the expected reduction in coronary morbidity and mortality. This apparent failure is perhaps not surprising when one considers the multifactorial nature of coronary artery disease and the different ways in which hypertension may affect the coronary circulation. Much debate has also centered on the antihypertensive therapy used in major trials in that it may in some way prevent the reduction in coronary mortality. However, thus far no clear evidence of a harmful effect has emerged. Reducing coronary mortality in hypertensive patients is a major challenge but one that can be effectively surmounted by approaching these different factors in a concerted manner. The ultimate goal must be to prevent the development of hypertension and left ventricular hypertrophy, but until such time as that can be achieved, the early detection of hypertension is mandatory. The optimal levels of systolic and diastolic blood pressures must be established. Studies on the more recent antihypertensive agents hold promise for a more specific effect on the atherosclerotic process as well as sustained control of arterial blood pressure. In this regard, it would seem essential to develop more precise ways of quantifying atherosclerosis and thus clarifying the nature of its relation to hypertension. Finally, management of hypertension must include precise assessment of the patient's overall cardiovascular risk status and appropriate and aggressive management of all risk factors for coronary artery disease.