ABO and Rhesus blood grouping in N.W.F.P.
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ABO Blood-Group System↗
Biomedical subjects
M Hussain
Publications and source records attributed to M Hussain.
Review of acute appendicitis at Civil Hospital, Abbottabad.
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Acute Disease↗
Chronic suppurative otitis media: a bacteriological study.
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Chronic Disease↗
Hemodynamic effects of nifedipine during upright exercise in stable angina pectoris and either normal or severely impaired left ventricular function.
The immediate effects of sublingual nifedipine (20 mg) were evaluated in 18 men with stable, exercise-related angina pectoris and angiographically confirmed coronary artery obstructions, stratified at the time of left ventricular (LV) angiography according to the degree of LV dysfunction supine at rest (Group 1: n = 9, left ventricular end-diastolic pressure [LVEDP] less than 20 mm Hg; Group 2: n = 9, LVEDP greater than 20 mm Hg). At rest, in the upright posture in both groups, nifedipine reduced the systemic vascular resistance (p less than 0.01). The systemic arterial mean (p less than 0.05) and diastolic (p less than 0.01) pressures were reduced despite an increase in the cardiac output (p less than 0.05). Heart rate was increased only in Group 1 (p less than 0.05). Pulmonary artery occluded pressure was unchanged in both groups. During upright bicycle exercise in all patients, compared to control measurements, systemic arterial pressure (p less than 0.01) and vascular resistance (p less than 0.05) were similarly reduced, while exercise cardiac output response and LV filling pressure did not change after nifedipine. Heart rate was increased in Group 1 (p less than 0.05) and decreased in Group 2 (p less than 0.05). Stroke volume during exercise after nifedipine decreased 1 ml/m2 in Group 1 (p greater than 0.05) and increased 2 ml/m2 in Group 2 (p greater than 0.05) compared to control measurements; the between-group difference in the exercise heart rate and stroke volume responses after nifedipine were significant at the 5% level.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Is the intrinsic sympathomimetic activity (ISA) of beta-blocking compounds relevant in acute myocardial infarction?
The relevance of the intrinsic sympathomimetic activity (ISA) of beta-blocking compounds to the clinical therapeutics of acute myocardial infarction was evaluated in 20 patients with an uncomplicated acute myocardial infarction by comparing the haemodynamic effects of equivalent beta-blocking doses of propranolol (non-cardioselective; no ISA) and pindolol (non-cardioselective; 50% ISA). Consecutive eligible male patients admitted to a Coronary Care Unit were randomised following a 1 h control period to two separate studies. In Study 1 the short-term dose-response effects of propranolol (1-8 mg) or pindolol (0.1-0.8 mg) were assessed. In Study 2 comparison of the effects of single i.v. propranolol (8 mg) and pindolol (0.8 mg) doses was undertaken over 6 h. Haemodynamic variables and thermodilution cardiac output were subsequently recorded to compare the effects of each drug on the circulation. The plasma concentrations of propranolol and pindolol were in the recognised therapeutic range. Both drugs were clinically well-tolerated, the changes induced in haemodynamic variables following each drug demonstrated effective beta-blockade. Within the limits of the experimental protocol, these data did not suggest definite haemodynamic advantage for ISA of pindolol in acute myocardial infarction. These findings are perhaps due to sympathetic activation in acute myocardial infarction attenuating the haemodynamic impact of ISA.
Adrenergic beta-Antagonists↗
Rest and exercise hemodynamic effects of sequential alpha-1-adrenoceptor (trimazosin) and beta-adrenoceptor (propranolol) antagonism in essential hypertension.
The efficacy of acute beta blockade in essential hypertension is limited by reflex vasoconstriction. The aim of this study was to determine whether the latter response was modified by prior selective alpha-1-adrenoceptor blockade. A single-blind, within-patient, placebo-controlled evaluation of the immediate hemodynamic effects of sequential alpha-1 (trimazosin)- and beta (propranolol)-adrenoceptor blockade was undertaken in 10 men (34 to 58 years) with previously untreated essential hypertension. The study commenced with a 4-minute control period of constant-load (600 to 900 kpm/min) upright bicycle exercise, and measurements were made before (control) and 30 minutes after intravenous trimazosin (2 mg/kg) and exercise was then repeated; measurements at rest were again made 4 minutes after intravenous propranolol (0.2 mg/kg) before a final exercise period. Trimazosin at rest reduced systolic and diastolic arterial pressure and systemic vascular resistance without change in heart rate, cardiac output, or left ventricular (LV) filling pressure. During upright bicycle exercise the reductions in blood pressure were sustained without change in their rest-to-exercise increments. Other circulatory variables did not differ from control values. At rest the addition of propranolol further reduced systolic arterial pressure. Heart rate and cardiac output fell and systemic vascular resistance increased to its pretreatment control value. During exercise the changes at rest were sustained and the rest-to-exercise increments in blood pressure, heart rate, and cardiac output were reduced. LV filling pressure was significantly increased. In conclusion, alpha-1-adrenoceptor blockade modified the adverse effects of acute beta blockade at rest but not during exercise.
Adult↗
Dose-response effects of cardioselective beta blockade in coronary artery disease.
The hemodynamic dose-response effects of intravenous acebutolol, a cardioselective beta-adrenoceptor antagonist with intrinsic sympathomimetic activity, were evaluated in 12 male subjects with angiographically confirmed coronary artery disease. At rest after a saline solution control period, four doubling intravenous boluses of acebutolol (logarithmic cumulative dosage of 20, 40, 80, and 160 mg) were injected at 4-min intervals; hemodynamic variables were recorded 2 to 4 min after each injection. Hemodynamic effects of the drug during steady-state exercise were evaluated by comparison of a control exercise period with observations made at the same workload (25W to 50W) after the maximum cumulative dose (160 mg). After the four intravenous boluses, plasma acebutolol concentrations rose in log-linear fashion and levels achieved (0.6 to 3.5 micrograms/ml) were within the range at which substantial pharmacodynamic activity is usually present (i.e., 0.02 to 0.2 microgram/ml). Compared with control measurements at rest after saline solution injection, these plasma concentrations of acebutolol resulted in a quadratic reduction in heart rate (maximum delta HR, -4 bpm) and a linear increase in pulmonary artery occluded pressure (maximum delta PAOP, +3 mm Hg) without change in systemic arterial pressure. There was a small reduction in cardiac output (delta cardiac index [CI], -0.2 l/min/m2). During steady-state supine bicycle exercise, there were significant reductions in systolic blood pressure (delta SBP, -15 mm Hg, or 9%) HR (-9 bpm or -9%), cardiac output (delta CI, -1.0 l/min/m2, or -18%), and increase in PAOP (+8 mm Hg, or +38%).(ABSTRACT TRUNCATED AT 250 WORDS)
Acebutolol↗
The effect on left ventricular performance of nifedipine and metoprolol singly and together in exercise-induced angina pectoris.
Clinical concern still exists regarding the potentially deleterious results of the combined negative inotropic effects of cardiac beta-adrenoceptor and slow calcium channel blockade in patients with impaired left ventricular function due to coronary heart disease. The haemodynamic effects of sublingual nifedipine (20 mg) and intravenous metoprolol (10 mg) singly and in combination were therefore studied in 20 patients with severe angina pectoris associated with angiographically documented coronary artery disease. The plasma concentrations of each drug at the time of the haemodynamic measurements were within the range associated with relief of exercise-induced anginal pain. Sitting at rest, nifedipine was associated with reductions in systemic arterial pressure (P less than 0.05), systemic vascular resistance (P less than 0.001), and increases in heart rate (P less than 0.01) and cardiac output (P less than 0.05) without significant change in the left heart filling pressure. In contrast, sitting at rest, metoprolol was associated with reductions in systemic blood pressure (P less than 0.05), heart rate (P less than 0.001) and cardiac output (P less than 0.05) and an increase in left heart filling pressure (P less than 0.01). After both drugs, similar directional changes were observed during upright bicycle exercise compared to the control exercise measurements. In combination, the negative inotropic effects of metoprolol were largely offset by the reduction of the systemic vascular resistance due to nifedipine. Conversely the reflex tachycardia following nifedipine was countered by metoprolol. Thus the combination reduced two of the major determinants of left ventricular oxygen consumption, namely heart rate and systemic blood pressure, at the expense of a small increase in left heart filling pressure. This may have explained the subjective improvement in anginal symptoms noticed by the majority of the patients. The combination of nifedipine and metoprolol was haemodynamically more advantageous both at rest and during exercise than either drug alone in our patients with depressed left ventricular function due to the coronary heart disease.
Adult↗
Enhanced haemodynamic effects of propranolol in acute myocardial infarction.
To evaluate the possible influence of sympathetic activation on the haemodynamic response to intravenous beta-blockade, the dose-response characteristics of three boluses of propranolol were evaluated in 8 patients with uncomplicated infarction and compared in a similar number of patients with stable angina. Following a control period, when haemodynamic stability was confirmed, propranolol 2, 2 and 4 mg (cumulative dosage 2, 4 and 8 mg) was injected into the central circulation at 15 min intervals. Despite close matching in baseline control haemodynamic variables between the groups, in stable angina, propranolol resulted in dose-related depression of cardiac output without change in systemic blood pressure, whereas following myocardial infarction the drug induced significantly greater falls in cardiac output (P less than 0.05) and a dose-related decrease in systemic blood pressure. Despite the greater effects of propranolol on cardiac output following myocardial infarction, the left ventricular filling pressure was increased to a lesser extent compared with stable angina. The explanation for this observation may reside in a greater susceptibility of the left ventricular wall to increase its compliance, under conditions of high sympathetic stimulation, following beta-blockade. These data support experimental and biochemical evidence of sympathetic activation in myocardial infarction; the hyperadrenergic state conditions an augmented haemodynamic response to competitive antagonism of sympathetic stimulation at cardiac beta-adrenoceptors.
Aged↗
The effects on left ventricular performance of nifedipine and verapamil in exercise-induced angina pectoris.
The differences between slow calcium blocking agents with respect to effects on heart rate, myocardial contractility and atrioventricular conducting time are well described; the relevance of such differences to the treatment of patients with impaired left ventricular function due to coronary heart disease is uncertain. The haemodynamic effects of equivalent hypotensive doses of nifedipine and verapamil were therefore compared in 20 patients with severe angina pectoris associated with angiographically documented coronary artery disease. The plasma concentrations of nifedipine (mean 57 +/- 19; range 27-77 ng/ml) and verapamil (mean 147 +/- 14; range 117-260 ng/ml) at the time of the haemodynamic measurements were of an order usually associated with substantial pharmacodynamic activity. Sitting at rest nifedipine resulted in reduction in systemic arterial pressure (P less than 0.05) and vascular resistance (P less than 0.01); both the heart rate (P less than 0.01) and cardiac output (P less than 0.05) increased without any significant change in the left heart filling pressure. In contrast, verapamil, which similarly reduced systemic blood pressure (P less than 0.05) and vascular resistance (P less than 0.01), increased cardiac output (P less than 0.05) and left heart filling pressure (P less than 0.05) without any change in heart rate. During upright bicycle exercise both drugs attenuated the angina induced in all subjects during the control exercise period. Despite reductions in systemic blood pressure and vascular resistance the cardiac output was unaltered on either drug at the same workload as in the control assessment. The reduction in exercise blood pressure following nifedipine induced a reflex tachycardia; this was not present, despite the similar hypotensive action, after verapamil.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
The effect of cimetidine on the relative cardioselectivity of atenolol and metoprolol in asthmatic patients.
The effects of chronic cimetidine therapy on the pharmacodynamic properties of atenolol and metoprolol were assessed in eight asthmatic patients using a placebo-controlled trial. When atenolol and metoprolol were administered at doses which achieved an equivalent degree of beta1-adrenoceptor blockade, metoprolol caused a significantly greater reduction in mean forced expiratory volume in one second (FEV1). This demonstrates the greater cardioselectivity of atenolol. The reductions in mean FEV1 induced by either atenolol or metoprolol were each unaffected by cimetidine. Plasma levels of each of the beta-adrenoceptor blockers were not affected by the addition of cimetidine. The FEV1 in one patient was further reduced when cimetidine was administered with metoprolol, although there was no corresponding change in plasma levels of drug. In this patient there was no such further reduction in FEV1 with atenolol. This study has not provided evidence for a pharmacodynamic interaction between cimetidine and either atenolol or metoprolol, but further studies are indicated.
Asthma↗
Haemodynamic dose-response effects of i.v. nicardipine in coronary artery disease.
The haemodynamic dose-response effects of the slow channel blocking agent nicardipine were evaluated in 10 male patients with angiographically confirmed coronary artery disease. At rest, following a similar control saline period, four doses of the drug (log cumulative dosage: 1.25, 2.5, 5.0 and 10.0 mg) were administered by i.v. infusion over a total duration of 40 min; haemodynamic variables were recorded in the 3-5 min following each 5 min infusion. During steady-state exercise the haemodynamic effects of the drug were evaluated by comparison of a control exercise period with observations made at the same workload (200-500 kpm) following the maximum cumulative dose (10 mg). Following the four i.v. infusions, the plasma nicardipine level increased log-linearly with the infused dose (r = 0.68). Compared with control measurements at rest after saline, these plasma concentrations (35 +/- 8 to 141 +/- 24 micrograms/l) resulted in a linear decrease in systemic blood pressure and vascular resistance with significant increase in cardiac index (maximum delta CI + 1.6 l min(-1) m(-2); P less than 0.01), stroke index (maximum delta SI + 11 ml/m2; P less than 0.01) and in pulmonary artery occluded pressure (maximum delta PAOP + 2 mm Hg; P less than 0.01). There was a significant increase in heart rate; the stroke work index was unchanged. During upright bicycle exercise the reduction in systemic blood pressure was accompanied by an increased exercise cardiac output without change in stroke index. The exercise pulmonary artery occluded pressure was unchanged compared with control observations, the stroke work index fell significantly (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Chemotherapy-induced interstitial pneumonitis during treatment of small cell anaplastic lung cancer.
Twelve cases of interstitial pneumonitis were seen in 50 patients (24%) treated with cyclophosphamide, methotrexate, and etoposide (VP-16-213) for small cell anaplastic lung cancer. The clinical course and pathologic characteristics were consistent with drug-induced pneumonitis in all 12 cases. One additional patient had concurrent histologic evidence of interstitial pneumonitis, pneumocystis infection, and perivascular metastases. Patients presented with severe dyspnea, hypoxemia, cough, fever, and bilateral interstitial infiltrates on chest films. The onset was rapid and unpredictable, following as little as one month or as much as five months of therapy. Nine patients recovered but there were three deaths in the acute period directly attributable to the drug-induced pneumonitis. Although the use of twice weekly oral methotrexate may have been a causative factor, a previously unsuspected drug interaction with etoposide may be the etiologic factor resulting in this unusually high incidence of pulmonary toxicity. The difficulty in establishing a diagnosis of interstitial pneumonitis in this group of patients with chronic lung disease and lung cancer is well known. The extent of morbidity and mortality seen in this study and the commercial availability of etoposide make earlier clinical recognition of this complication imperative.
Adrenal Cortex Hormones↗
A four-year experience with preoperative noninvasive carotid evaluation of two thousand twenty-six patients undergoing cardiac surgery.
From January 1979 through December 1982, 2026 patients scheduled to undergo open heart surgery were evaluated by a preoperative battery of noninvasive carotid tests including phonoangiography, oculopneumoplethysmography, pulse-timing oculoplethysmography, periorbital Doppler examination, and during the last 12 months, continuous-wave Doppler ultrasonography with spectral analysis. The incidence of hemispheric neurologic deficit following cardiac surgery in the 47 patients with carotid disease was 14.9%; the incidence in patients with no carotid disease was 1.9% (p less than 0.001). Fourteen of the 47 patients were not candidates for carotid surgery because of unilateral occlusion in 13 and bilateral occlusion in one. Three of the 14 (21.4%) had intraoperative strokes on the appropriate side. Thirty-three of the 47 had operable carotid disease. Four with unilateral stenosis had no carotid surgery; one had a postoperative deficit on the side referable to the nonstenotic artery. Eighteen with unilateral stenosis underwent simultaneous cardiac and carotid surgery; one (5.6%) had a transient deficit. Seven patients with bilateral stenosis underwent cardiac and unilateral carotid surgery; no deficits occurred. Four patients with unilateral stenosis and contralateral occlusion underwent combined surgery; one had a transient ischemic attack and one a fatal stroke, both referable to the hemisphere ipsilateral to the occlusion. It appears that the presence of carotid disease increased the risk of stroke during heart surgery. Proof that carotid endarterectomy lowers this risk awaits a prospective randomized trial.
Angiography↗
Comparative haemodynamic dose-response effects of intravenous propranolol, acebutolol and penbutolol in angina pectoris.
The relevance of the ancillary pharmacological properties of intrinsic sympathomimetic activity (ISA) and cardioselectivity to the haemodynamic profile following intravenous beta-blockade was examined in a randomised study of propranolol (16 mg), acebutolol (160 mg) or penbutolol (4 mg) in 30 patients with stable angina pectoris. Haemodynamic measurements were undertaken at rest and during four minutes steady-state supine bicycle exercise (25 to 50 W), load limited to the angina threshold, before and after each drug. The randomised groups were statistically similar for major haemodynamic and clinical variables. The plasma concentrations achieved for each drug were in the therapeutic range. At rest, propranolol resulted in greater reductions in resting cardiac output and greater increase in pulmonary artery occluded pressure compared with acebutolol and penbutolol. During the sympathetic stimulus of dynamic exercise, penbutolol resulted in less depression of exercise cardiac performance than either acebutolol or propranolol. These observations are compatible with previous studies which suggested that the possession of ISA by a beta-blocking drug offset the depression of cardiac performance following intravenous beta-blockade; the benefits of ISA on haemodynamic profile appeared maximum at rest and were reduced or abolished during dynamic exercise.
Acebutolol↗
Haemodynamic dose-response effects of i.v. verapamil in coronary artery disease.
As an aid to clinical therapeutic decisions, the haemodynamic dose-response effects following intravenous verapamil were evaluated in ten male patients with angiographically confirmed and stable coronary artery disease. Sitting at rest, following a control period with four i.v. boluses of saline, four equivalent boluses of verapamil (logarithmic cumulative dosage; 2, 4, 8 and 16 mg) were administered at four minute intervals; haemodynamic variables were recorded two to four minutes following each i.v. injection. The haemodynamic effects of the drug during upright bicycle exercise were evaluated by comparison of measurements made during a control steady-state exercise period with observations made at the same upright exercise workload (25 to 75 W) immediately following the maximum cumulative dose (16 mg). Following the four i.v. boluses, the plasma verapamil concentrations showed a log-linear increase (r = 0.82; p less than 0.001); the levels achieved (26 +/- 2 to 147 +/- 14 micrograms/l) were within the range at which substantial pharmacodynamic activity has been shown to be present. At rest, compared with control measurements after saline, these plasma concentrations of verapamil were associated with linear decreases in systemic vascular resistance (maximum delta SVR -720 dyne X s X cm-5/m2; p less than 0.01) and blood pressure (maximum delta MBP -8 mmHg; p less than 0.05) and linear increases in cardiac index (maximum delta CI +0.4 l/min/m2; p less than 0.05) and in pulmonary artery occluded pressure (maximum delta PAOP +3 mmHg; p less than 0.05). There was no significant trend of change in the heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Testicular feminisation syndrome.
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Adult↗