Misuse of calcium antagonists after myocardial infarction.
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Adrenergic beta-Antagonists↗
Biomedical subjects
F G Dunn
Publications and source records attributed to F G Dunn.
Significance of ventricular arrhythmias in systemic hypertension with left ventricular hypertrophy.
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.
Adult↗
Impact of regression of left ventricular hypertrophy on cardiac function in hypertension.
It is now established that regression of left ventricular hypertrophy (LVH) occurs following reduction of arterial pressure in patients with hypertension. A number of factors contribute towards this regression, including the fall in blood pressure itself, the drug therapy given, and the pre-existing degree of hypertrophy. LVH is in some senses a beneficial adaptive response in terms of systolic function, and therefore it is important to clarify whether or not regression of hypertrophy is damaging to cardiac function. Overall assessment of these effects has been more difficult because the antihypertensive drug therapy and the changes in blood pressure also contribute to left ventricular function. Current data indicate that systolic function is maintained both at rest and following exercise but not necessarily improved. In contrast, diastolic function in some but not all studies, has been shown to have been improved. Recent information has allayed fears that regression of LVH may cause a deterioration in function if blood pressure is allowed to return to its pretreatment levels. It would appear that in this situation function is maintained both at rest and during exercise. Finally, the assessment of cardiac function following regression of hypertrophy remains a surrogate end-point. The key information required remains the influence of regression of hypertrophy and its alteration in function on morbidity and mortality in patients with hypertension.
Antihypertensive Agents↗
Symptomatic and silent myocardial ischaemia in hypertensive patients with left ventricular hypertrophy.
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.
Adult↗
Leaking false aneurysm of right coronary saphenous vein graft; successful treatment by percutaneous coil embolisation.
An unusual complication after aortocoronary bypass grafting (CABG) is described in which a false aneurysm of the saphenous vein graft to the right coronary artery (RCA) developed and caused profuse intermittent bleeding through the sternotomy wound. The aetiology of this condition is uncertain but it could occur whenever a suture line is present especially in the presence of infection. The diagnosis was made non-invasively by a contrast enhanced computed tomogram and was subsequently confirmed by selective coronary bypass angiography. The pseudoaneurysm was successfully obliterated by coil embolisation of the right coronary graft, which stopped the bleeding immediately and was followed by rapid wound healing.
Aneurysm, False↗
Monitoring of streptokinase resistance titre in acute myocardial infarction patients up to 30 months after giving streptokinase or anistreplase and related studies to measure specific antistreptokinase IgG.
OBJECTIVE: To examine the induction of antistreptokinase antibodies after giving streptokinase or anistreplase to patients with acute myocardial infarction. DESIGN: Patients were randomly allocated to receive either 1.5 x 10(6) IU, streptokinase or 30U anistreplase in a double blind study. Blood samples were collected immediately before treatment and subsequently at intervals up to 30 months; plasma samples were assayed for streptokinase resistance titre (functional assay) and streptokinase binding by IgG (microradioimmunoassay). SETTING: Cardiology department in a general hospital. PATIENTS: 128 consecutive eligible patients. Samples were collected for up to one year according to a prospective design: a subsection of 47 patients was selected for intensive study over the first 14 days. After one year, all available patients (67) were sampled on one further occasion. RESULTS: Antibody responses to streptokinase and anistreplase were similar. Streptokinase resistance titres exceeded pretreatment concentrations five days after dosing, and values peaked at 14 days. By 12 months after dosing, 92% of resistance titres (n = 84) had returned to within the pretreatment range. Antistreptokinase IgG concentrations also exceeded baseline concentrations within five days and peaked at 14 days. Half of the individual values had returned to within the pretreatment range by 12 months (n = 84) and 89% by 30 months (n = 18). CONCLUSION: Although we cannot be sure of the clinical significance, because of the increased likelihood of resistance due to antistreptokinase antibody, streptokinase and anistreplase may not be effective if administered more than five days after an earlier dose of streptokinase or anistreplase, particularly between five days and 12 months, and increased antistreptokinase antibody may increase the risk of allergic-type reactions.
Adult↗
Long-term amiodarone therapy raises serum cholesterol.
Serum total cholesterol and triglyceride levels were measured in 12 patients before and 3.6 and 9 months after treatment with amiodarone. In addition, we monitored serum T4, T3, reverse T3 and TSH levels. Amiodarone and its desethyl metabolite levels were measured on each occasion. Serum total cholesterol and T4 levels rose from 5.95 mmol/l, and 102.7 mmol/l respectively at baseline to 6.95 and 115.8 at 6 months and reverse T3 increased at 3, 6 and 9 months from baseline. Serum triglycerides did not change. No relationship existed between cholesterol, T4 and T3 and amiodarone (or its metabolite) levels nor between cholesterol and thyroid hormone levels. These data demonstrate that amiodarone therapy is associated with an elevation in serum cholesterol. This may have clinical implications in view of the current widespread use of the drug.
Adult↗
Left ventricular hypertrophy in hypertension.
Major advances in left ventricular hypertrophy (LVH) and hypertension have occurred in recent years. The ability to diagnose LVH has been improved by echocardiography, and with this technique it has been shown that evidence of LVH is an important independent risk factor for cardiovascular disease. The major cause of death in patients with hypertension and LVH is coronary artery disease. Therefore an understanding of the interrelationships between these two disorders is fundamental, and it is now clear that the hypertrophied ventricle is vulnerable to myocardial ischemia. Appreciation of the mechanisms of sudden death has also increased, although the exact situation in patients with LVH remains to be clarified. Regression of LVH is known to occur with the use of several different antihypertensive drugs. Recent studies indicate that the calcium blocking agent nicardipine, in addition to beta-blocking drugs and angiotensin-converting enzyme inhibitors, brings about LVH regression without any deterioration of left ventricular function. However, further studies are needed to assess the long-term benefits of this regression.
Calcium Channel Blockers↗
Doppler evaluation of a left atrial myxoma.
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.
Echocardiography, Doppler↗
Systolic and diastolic function following regression of left ventricular hypertrophy in hypertension.
Echocardiography has demonstrated that regression of left ventricular hypertrophy (LVH) can occur following control of blood pressure, although the role of individual drugs in promoting this regression remains less clear. Since LVH in hypertension is an adaptive response to the increased afterload, and therefore serves to normalize wall stress, it is important to establish the effects of hypertrophy regression on cardiac function. Assessment of these effects, however, is complicated by the contributions of alteration in loading conditions and drug therapy to left ventricular function. Since systolic function is normal in LVH, it is not surprising that regression leads to no significant change in commonly measured indices of contractile function. Abnormalities of diastolic function, on the other hand, occur as a consequence of both hypertension and LVH, and reversal of these abnormalities might, therefore, be expected to lead to an improvement in diastolic function. This is indeed the case, although not in all reported studies. Only recently has information emerged on the effects of regression of LVH on function when blood pressure is allowed to return to its pretreatment level following discontinuation of antihypertensive therapy. Such trials, although requiring careful monitoring, are the only way of providing information on the effects of regression itself on left ventricular function. The implications of LVH regression and its attendant changes in function remain to be determined.
Adaptation, Physiological↗
A comparison of the pharmacokinetic properties of streptokinase and anistreplase in acute myocardial infarction.
1. The pharmacokinetics of streptokinase (SK) and anistreplase in conventional dosage regimens of 1.5 x 10(6) i.u. of SK infused over 60 min and 30 units of anistreplase over 5 min were studied in 24 consecutive patients presenting with acute myocardial infarction, using a functional bioassay to assess concentrations. 2. The two agents were found to have similar volumes of distribution (5.68 and 5.90 l), but SK was cleared significantly more rapidly than anistreplase, resulting in a shorter terminal phase half-life (0.61 vs 1.16 h) and a shorter mean residence time (0.76 vs 1.55 h).
Aged↗
A pilot study of the efficacy and safety of bolus administration of alteplase in acute myocardial infarction.
OBJECTIVE: To examine the efficacy, safety, and the pharmacokinetic profile of a bolus dose administration regimen of alteplase in the treatment of acute myocardial infarction. DESIGN: An open pilot study. SETTING: District general hospital. PATIENTS: 33 suitable consecutive patients presenting within six hours of the onset of symptoms who satisfied the electrocardiographic criteria for acute myocardial infarction. INTERVENTIONS: Two intravenous boluses of 35 mg alteplase, 30 minutes apart. MAIN OUTCOME MEASURES: Angiographic coronary patency at 90 minutes and 24 hours. Plasma alteplase concentration-time profile and pharmacokinetic analysis. RESULTS: Coronary patency at 90 minutes: 26 of 30 arteries (87%, 95% confidence interval (CI) 74-99%). Coronary patency at 24 hours: 24 of 29 arteries (83%, CI 69-97%). Mean (SD) plasma tissue plasminogen activator (t-PA) concentration reached 4434.8 (2117.8) and 4233.3 (2217.5) ng/ml within 10 minutes of each bolus and fell to 425.8 (288.3) ng/ml between boluses. The estimated peak concentrations at two minutes after boluses were 12,389 (8580) ng/ml and 10,811 (6802) ng/ml. The derived pharmacokinetic variables were volume of distribution 3.11 (1.89) 1, clearance 21.3 (9.3) 1/h, half life 5.9 (1.7) minutes. CONCLUSIONS: This simple administration regimen achieved brief, high concentrations of plasma t-PA that were well tolerated. The regimen was associated with a high coronary patency rate at 90 minutes that was well maintained at 24 hours.
Adult↗
Hypertension and coronary artery disease. Can the chain be broken?
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.
Animals↗
Angiographic patency study of anistreplase versus streptokinase in acute myocardial infarction.
128 patients with acute myocardial infarction of duration 6 h or less were randomised in double-blind fashion to receive 30 U anistreplase over 5 min or 1.5 MU streptokinase over 1 h, both intravenously. Angiographic patency was assessed 90 min and 24 h from the start of therapy. 55% of patients who received anistreplase and 53% of patients who received streptokinase had patent infarct-related arteries (TIMI grade 2-3) at 90 min (95% CI 42-68% and 40-66%, respectively). At 24 h 81% and 87.5% of arteries were patent respectively (95% CI, 71-91% and 83.5-91.5%). Time to therapy had no significant effect on patency rates. There was one early reocclusion within 24 h in each treatment group and clinical evidence of reocclusion was recorded between 24 h and hospital discharge in a further 5 patients (streptokinase 3, anistreplase 2). With these regimens, therefore, anistreplase and streptokinase gave the same patency rates.
Adult↗
Colour Doppler flow mapping in the diagnosis of traumatic ventricular septal defect.
The use of colour Doppler flow mapping allows noninvasive diagnosis and gives haemodynamic information on the severity of ventricular septal defects. We describe the case of a man with delayed presentation of a traumatic ventricular septal defect in whom colour Doppler flow mapping permitted conservative management after accurate noninvasive diagnosis.
Adult↗
Left ventricular hypertrophy and mortality in hypertension: an analysis of data from the Glasgow Blood Pressure Clinic.
Three thousand seven hundred and eighty-three patients with non-malignant hypertension attending the Glasgow Blood Pressure Clinic between 1968 and 1983 were followed prospectively for an average of 6.5 years. Left ventricular hypertrophy (LVH) was present at the outset in 34.5% of the men, and 12.8% had ST-T changes. The corresponding figures for women were 21.5% and 8.8%. The prevalence of LVH increased with the severity of hypertension and was higher for a given blood pressure level in men than in women. All-cause age-adjusted mortality, expressed as deaths per 1000 patient-years, was 27.6 for men with normal electrocardiographs, 43.2 for men with LVH only (P less than 0.001) and 56.9 for men with LVH and ST-T changes (P less than 0.001). Similar trends were seen in women. The excess risk associated with LVH, with or without ST-T changes, could not be explained by age, increased blood pressure at referral to the clinic, or smoking habit, when these factors were considered either separately or in combination (regression analysis). Thus, our study demonstrates that LVH, with or without ST-T changes is an independent risk factor for mortality in hypertensive patients.
Age Factors↗
Regression of left ventricular hypertrophy in patients with hypertension.
Left ventricular hypertrophy is an ominous prognostic factor for all the cardiovascular complications of hypertension. Treatment has undoubtedly improved the outlook, particularly in patients with congestive cardiac failure. It has recently been shown that the hypertrophy process itself can be regressed by control of hypertension. The principal factor of importance in this regression process is the fall in blood pressure. Although experimental studies suggest that the renin-angiotensin-aldosterone (RAA) system and the sympathetic nervous system (SNS) both play a role in regression, clinical studies in this regard are suggestive but not conclusive. Left ventricular function appears well preserved with the control of blood pressure and parallel reduction in pressure and left ventricular mass is likely to have no adverse effect on myocardial perfusion. The implications of regression of hypertrophy and the patient's long term prognosis have not yet been determined.
Antihypertensive Agents↗