Search PubMed⌕ Search

Biomedical subjects

B G Firth

Publications and source records attributed to B G Firth.

At least 55 records · Page 3Linked to original sources
PubMed1983

Effects of provocation on transcardiac thromboxane in patients with coronary artery disease.

Thromboxane A2 exerts powerful effects on vascular smooth muscle tone and platelet aggregability. Previous studies have demonstrated increases in transcardiac thromboxane B2 (a stable thromboxane A2 metabolite) in patients with unstable angina and recent chest pain. To determine whether these increases in transcardiac thromboxane B2 are unique to the unstable anginal syndrome or are merely a consequence of ongoing myocardial ischemia, simultaneous ascending aortic and coronary sinus blood samples were obtained for quantitation of thromboxane B2 in 52 patients with a history of chest pain. Provocation was performed with (1) rapid cardiac pacing in 23 patients, (2) cold pressor stress in 19 patients, and (3) sustained isometric exertion in 10 patients. Of the 52 patients, only 5 had a substantial (greater than 3-fold) increase in coronary sinus thromboxane B2 in response to provocation: 1 had unstable angina and chest pain during the previous 48 hours and 4 had a myocardial infarction within the previous 6 weeks. Similarly, only 7 had a greater than 3-fold increase in the coronary sinus/aortic thromboxane B2 ratio in response to provocation: 1 had unstable angina and recent chest pain, 5 had a recent myocardial infarction, and 1 had both of these. There were no other clinical features unique to these patients. The remaining patients with similar diagnoses did not develop a marked increase in coronary sinus thromboxane B2 or the coronary sinus/aortic thromboxane B2 ratio with provocation. None of the 35 patients with stable ischemic heart disease or nonischemic chest pain syndromes had a substantial increase in coronary sinus thromboxane B2 or the coronary sinus/aortic thromboxane B2 ratio (p less than 0.001 for both coronary sinus thromboxane B2 and the coronary sinus/aortic thromboxane B2 ratio in comparison with the 17 patients with recent unstable angina or myocardial infarction). Thus, generous amounts of thromboxane B2 are released into the coronary circulation after provocation in some patients with unstable angina or recent myocardial infarction but not in those with stable ischemic heart disease or nonischemic chest pain syndromes.

Adult↗
PubMed1983

Alterations in left ventricular volumes and ejection fraction during atrial pacing in patients with coronary artery disease: assessment with radionuclide ventriculography.

The present study was performed to determine the utility of radionuclide ventriculography (RNV) in conjunction with atrial pacing in the identification of individuals with coronary artery disease. Accordingly, left ventricular end-diastolic volume index, end-systolic volume index, ejection fraction, and regional wall motion were measured with radionuclide ventriculography before and during atrial pacing in 37 patients: 27 with and 10 without (control subjects) coronary artery disease. In the control subjects, pacing caused a decrease in end-diastolic volume index (77 +/- 19 [mean +/- SD] ml/M2 at rest, 50 +/- 18 ml/M2 at peak pacing; p less than 0.001), a decrease in end-systolic volume index (34 +/- 14 ml/M2 at rest, 19 +/- 9 ml/M2 at peak pacing; p less than 0.001), an increase in ejection fraction (0.61 +/- 0.11 at rest, 0.66 +/- 0.11 at peak pacing; p = 0.006); and no deterioration in wall motion. In 16 patients with coronary artery disease who developed ECG and/or metabolic evidence of ischemia during pacing, end-diastolic volume index decreased (87 +/- 26 ml/M2 at rest, 69 +/- 24 ml/M2 at peak pacing; p less than 0.001), end-systolic volume index was unchanged (43 +/- 20 ml/M2 at rest, 44 +/- 21 ml/M2 at peak pacing; p = NS), ejection fraction decreased (0.55 +/- 0.12 at rest, 0.40 +/- 0.14 at peak pacing; p less than 0.001), and new wall motion abnormalities developed in 14. In 11 patients with coronary artery disease but no ECG or metabolic evidence of ischemia, pacing caused a decrease in end-diastolic volume index (80 +/- 26 ml/M2 to 61 +/- 31 ml/M2; p less than 0.001), a decrease in end-systolic volume index (36 +/- 17 ml/M2 to 28 +/- 20 ml/M2; p = 0.002), no change in ejection fraction (0.60 +/- 0.11 to 0.60 +/- 0.13; p = NS), and new wall motion abnormalities in four. Although the specificity of these scintigraphic measurements for the identification of patients with coronary artery disease was excellent (1.0), the combined sensitivity of all scintigraphic measurements was high only if ECG or metabolic evidence of ischemia was present: 0.94 in patients with evidence of ischemia but only 0.36 in those without ischemia. Thus radionuclide ventriculography during incremental atrial pacing is useful in the identification of patients with coronary artery disease only if ischemia is induced.

Cardiac Output↗
PubMed1983

Prognostic value of resting and submaximal exercise radionuclide ventriculography after acute myocardial infarction in high-risk patients with single and multivessel disease.

In patients who survive the acute phase of myocardial infarction, those with multivessel coronary artery disease generally have a worse prognosis than those with single-vessel disease. However, some patients with significant multivessel stenoses have a good prognosis, whereas some with a significant single-vessel stenosis have a poor prognosis. Thus, although definition of coronary anatomy may be helpful, it is a not a fail-safe prognosticator. In this retrospective analysis, the association of abnormalities at rest and during submaximal exercise testing with radionuclide ventriculography after acute myocardial infarction with major cardiac complications (death, recurrent infarction, severe angina or congestive heart failure) in the ensuing 6 months was assessed in patients with single and multivessel disease. Coronary angiography and submaximal exercise testing with radionuclide ventriculography were performed within 3 months of each other in 42 patients. Eleven of the 16 patients with single-vessel coronary stenosis had major cardiac complications. The subsequent course of these 16 patients was correctly predicted by left ventricular ejection fraction (LVEF) less than or equal to 0.40 in 8 patients, by LVEF less than 0.55 in 7 patients, by failure of LVEF to increase by 0.05 units in 13 patients, and by an increase in left ventricular end-systolic volume index (LVESVI) during exercise greater than 5% above baseline in 11 patients. Of the 26 patients with multivessel coronary artery disease, 24 had major cardiac complications. The subsequent course of these 26 patients was correctly predicted in 13 by LVEF less than or equal to 0.40, in 20 by LVEF less than 0.55, in 25 by a failure of LVEF to increase by 0.05 units during exercise, and in 20 by an increase in LVESVI by greater than 5% during exercise. Thus, submaximal exercise testing with radionuclide ventriculography may provide valuable prognostic information concerning the occurrence of major cardiac events after myocardial infarction not only in patients with multivessel disease, but also in those with single-vessel disease. Exercise-induced abnormalities of left ventricular function may have greater prognostic importance than the delineation of coronary arterial anatomy or the assessment of residual left ventricular function at rest.

Adult↗
PubMed1983

Symptomatic, electrocardiographic, metabolic, and hemodynamic alterations during pacing-induced myocardial ischemia.

Atrial pacing has been used to assess the physiologic impact of coronary artery disease (CAD). Several variables have served as markers of pacing-induced myocardial ischemia, but their specificities and sensitivities are unknown. Accordingly, in 28 patients, incremental atrial pacing was performed. Of the 28, 10 had no CAD. The left ventricular ejection fraction (LVEF) (by gated equilibrium blood pool scintigraphy) increased in this group (0.60 +/- 0.11 [mean +/- standard deviation] before pacing to 0.67 +/- 0.13 at peak-pacing, p = 0.002). In no patient did left ventricular end-diastolic pressure increase by greater than 5 mm Hg. No patient had lactate production, and 2 (20%) had electrocardiographic S-T segment depression greater than or equal to 0.1 mV. Four (40%) had chest pain with atrial pacing. In the remaining 18 patients with CAD, atrial pacing caused a decrease in LVEF greater than or equal to 0.05 (0.46 +/- 0.10 to 0.33 +/- 0.09, p less than 0.001) and new segmental wall motion abnormalities in all, indicating pacing-induced myocardial ischemia. Only 8 (44%) had an increase in left ventricular end-diastolic pressure of greater than 5 mm Hg, and only 9 (50%) had lactate production. Ten (56%) had ischemic electrocardiographic changes, and 12 (67%) had chest pain. Thus, the electrocardiographic, metabolic, and hemodynamic alterations that may accompany pacing-induced ischemia are specific but relatively insensitive markers of ischemia. In contrast, chest pain during atrial pacing is a nonspecific occurrence, appearing with similar frequency in normal subjects and patients with CAD and pacing-induced ischemia.

Adult↗
PubMed1983

Independence of oxygen consumption and systemic oxygen transport in patients with either stable pulmonary hypertension or refractory left ventricular failure.

Recent studies have suggested that oxygen consumption (VO2) may be dependent on systemic oxygen transport (SOT) in patients with the adult respiratory distress syndrome. To evaluate this relationship in patients with chronically impaired SOT, 2 groups underwent control right heart catheterization. Twenty-six patients with pulmonary hypertension (Group I) were then reevaluated after 48 h of treatment with a vasodilator, either hydralazine or nifedipine. Nine patients with refractory left ventricular failure (Group II) were first studied using nitroprusside, and 24 h later were begun on a double-blind drug protocol using either minoxidil or hydralazine. A significant correlation existed between control SOT and VO2 in both groups (r = 0.65, p less than 0.001). There were no changes in either group, however, in VO2 with vasodilator therapy, despite significant increases in cardiac output and SOT. We conclude that although resting oxygen consumption may be correlated with systemic oxygen transport when SOT is at low levels in stable patients with chronically impaired SOT, VO2 appears to be independent of SOT when oxygen delivery is increased by the administration of vasodilators.

Biological Transport↗
PubMed1983

Treatment of primary pulmonary hypertension with nifedipine. A hemodynamic and scintigraphic evaluation.

To evaluate the potential value of nifedipine treatment for primary pulmonary hypertension, hemodynamic and scintigraphic measurements were made before and 15 to 30 minutes after nifedipine, 10 to 20 mg, was given sublingually to nine patients. Nifedipine treatment increased cardiac output (mean +/- SD, 3.6 +/- 1.7 to 5.3 +/- 2.8 L/min, p less than 0.001) and decreased mean aortic pressure (99 +/- 19 to 85 +/- 12 mm Hg, p less than 0.001) and total pulmonary and total systemic resistances (1605 +/- 787 to 1025 +/- 540 dyn X s X cm-5 and 2761 +/- 1557 to 1591 +/- 823 dyn X s X cm-5, respectively; p less than 0.005). Heart rate and mean pulmonary arterial pressure did not change significantly. Right ventricular end-diastolic volume decreased 10% (p = 0.01), end-systolic volume decreased 15% (p less than 0.01), and right ventricular ejection fraction increased 18% (p less than 0.05) in eight patients. After 4 to 14 months (mean, 7.3 +/- 3.8) of treatment with nifedipine, 40 to 120 mg/d, in six patients, cardiac output increased (3.6 +/- 2.0 to 5.0 +/- 1.8 L/min, p less than 0.01) and total pulmonary resistance decreased (1572 +/- 730 to 987 +/- 586 dyn X s X cm-5, p = 0.025), whereas pulmonary arterial pressure remained unchanged (59 +/- 23.2 to 55 +/- 28.6 mm Hg, p greater than 0.05) compared with baseline values. We conclude that nifedipine therapy may be useful in the chronic management of patients with primary pulmonary hypertension.

Adolescent↗
PubMed1982

The myocardial oxygen supply/demand ratio in patients with and without coronary artery disease.

This study was performed to assess the relationship between coronary sinus blood flow (by thermodilution) and myocardial oxygen demand (heart rate-systolic arterial pressure double product) during atrial pacing in patients with and without coronary artery disease. In 11 individuals with coronary artery disease, pacing was performed to ischemia, as reflected by electrocardiographic changes or lactate production; 8 patients without coronary artery disease served as controls. Coronary sinus blood flow (in ml/min) was similar for the two groups at rest. However, the increase in coronary blood flow from rest to peak pacing was less (P = 0.025) in those with coronary artery disease (50 +/- 26 ml/min) than in controls (79 +/- 26 ml/min). The ratio of coronary sinus blood flow to double product was the same at rest in both groups (11.1 +/- 2.2 x 10(-3) controls, 11.6 +/- 2.7 x 10(-3) coronary artery disease; NS). At peak pacing, it was unchanged in the controls (10.4 +/- 2.0 x 10(-3)) but fell in those with coronary artery disease (9.0 +/- 2.5 x 10(-3); P = 0.002). The aortic-coronary sinus oxygen content difference was similar at rest in both groups and did not change in response to pacing in either group. Thus, in response to augmented myocardial oxygen demand, patients without coronary artery disease have an appropriate increase in coronary blood flow and myocardial oxygen supply, while in those with coronary artery disease who develop ischemia the increment in myocardial blood flow (and oxygen supply) is inappropriately low.

Adult↗
PubMed1982

Oxygen consumption in adult patients during cardiac catheterization.

The determination of cardiac output by the Fick principle requires the quantitation of the arteriovenous oxygen (O2) content difference across the pulmonary bed and the O2 consumption. Since a correct measurement of O2 consumption may be difficult, an assumed value is sometimes substituted into this equation. Despite this practice, there is no appropriate reference standard for O2 consumption applicable to the adult catheterization laboratory. Therefore, we determined O2 consumption in 108 patients (69 men and 39 women, mean age, 49 years) at the time of catheterization by multiplying the arteriovenous content difference by the indicator dilution cardiac output, thereby eliminating errors related to the collection and analysis of the timed collection of expired air. O2 consumption index (O2 consumption/m2 of body surface area) averaged 126 +/- 26 ml/min/m2 (mean +/- SD), but there was wide variability(65-250 ml/Min/m2). O2 consumption was not affected by patient age or sex but was lower in those who were mildly sedated before catheterization (sedated, 121 +/- 22 ml/Min/m2; nonsedated, 132 +/- 28 ml/min/m2; p = 0.023). Thus, O2 consumption varies greatly among adults at the time of cardiac catheterization, so that any attempt at estimating this variable is fraught with major potential error.

Adult↗
PubMed1982

Influence of blood sampling site and technique on thromboxane concentrations in patients with ischemic heart disease.

Thromboxane A2 may play a role in coronary arterial spasm, unstable angina, myocardial infarction, cardiac arrhythmias, and sudden death. Although previous studies have examined peripheral, aortic, and coronary sinus concentrations of its stable metabolite, thromboxane B2 (TxB2), it is unknown, first, if blood sampling through long catheters alters the concentration of TxB2 and second, if peripheral levels of this prostanoid reflect its intracoronary production and release. In order to answer these questions, paired blood samples were obtained through an 18-gauge needle and a No. 7 or 8 French 110 to 125 cm catheter from the arterial (14 patients) and venous (16 patients) circulations; in addition, coronary sinus and peripheral venous samples were obtained in 16 patients and aortic samples were obtained in 14 of these patients. All samples were analyzed to TxB2 by radioimmunoassay. Blood sampling through long catheters did not systematically alter the concentrations of arterial TxB2 (needle, 85.5 +/- 67.5 pg/ml [mean +/- SD]; catheter, 62.3 +/- 40.9 pg/ml; p = 0.20) or venous TxB2 (needle, 182.5 +/- 170.5 pg/ml; catheter, 521.4 +/- 1536.0 pg/ml; p = 0.39). Peripheral venous TxB2 levels did not correlate with TxB2 levels in coronary sinus (r = 0.01) or the TxB2 coronary sinus/aortic ratios (r = 0.21). Thus blood sampling through long catheters across the coronary bed is both a reliable and necessary method for assessing intracoronary TxB2 production in patients with ischemic heart disease.

Adult↗
PubMed1982

Continuous electrocardiographic monitoring in patients with unstable angina pectoris: Identification of high-risk subgroup with severe coronary disease, variant angina, and/or impaired early prognosis.

We assessed the value of two-channel Holter monitoring during the initial hours of hospitalization in patients with unstable angina pectoris (UAP) to identify those with severe coronary artery disease (CAD), variant angina, and/or poor prognosis over the next 3 months. Accordingly, 116 UAP patients had Holter monitoring for 27 +/- 7 (mean +/- SD) (range 12 to 50) hours following hospitalization. Of these, 24 evolved myocardial infarction (MI) during monitoring and 92 did not. Transient ST segment alterations occurred in 21 of the 92. Of these 21, 4 had variant angina, were treated with calcium antagonists, and did well. Each of the remaining 17 had severe fixed CAD (left main or three-vessel) (n = 12) and/or poor prognosis over the 3 months after discharge as manifested by death (n = 1), MI (n = 3), and/or severe angina (n = 3). In contrast, 71 patients did not demonstrate transient ST segment alterations: none had variant angina (p less than 0.001), nine had left main or three-vessel CAD (p less than 0.001), and 50 were alive and well 3 months after discharge (p less than 0.001). Ventricular tachycardia (VT) was demonstrated by Holter monitor in 5 of the 92 patients: four had three-vessel CAD and the other had severe persistent angina. Thus in patients hospitalized with unstable angina, transient ST segment alterations and/or VT on Holter monitor are specific predictors of "high-risk" subgroup UAP patients with left main or three-vessel CAD, variant angina, and/or impaired 3-month prognosis.

Aged↗
PubMed1982

Effect of increasing heart rate in patients with aortic regurgitation. Effect of incremental atrial pacing on scintigraphic, hemodynamic and thermodilution measurements.

This study was performed to assess the effect of pacing-induced tachycardia in patients with aortic regurgitation. In 12 patients (5 men and 7 women with a mean age of 53 years) with aortic regurgitation, left ventricular end-diastolic and end-systolic volume indexes were measured with multigated equilibrium blood pool imaging, and forward cardiac index was determined with thermodilution, both at rest (mean heart rate +/- standard deviation 72 +/- 8 beats/min) and during atrial pacing at 100 and 120 beats/min. Pacing caused a decremental reduction in left ventricular end-diastolic and end-systolic volume indexes and radionuclide-determined stroke volume index but no change in radionuclide-determined cardiac index or left ventricular ejection fraction. Forward cardiac index increased incrementally from the baseline value at rest to that at 120 beats/min despite a decremental reduction in stroke volume index. There was a stepwise decrease in regurgitant volume/stroke (46 +/- 20 ml/m2 at baseline, 27 +/- 15 at 120 beats/min; p less than 0.05) but no change in regurgitant volume/min (3.38 +/- 1.80 liters/min per m2 at baseline, 3.22 +/- 1.78 at 120 beats/min; difference not significant [NS]) or regurgitant fraction (0.54 +/- 0.13 at baseline, 0.49 +/- 0.13 at 120 beats/min; NS). Mean femoral arterial, pulmonary arterial and pulmonary capillary wedge pressures did not change with pacing.

Aortic Valve Insufficiency↗
PubMed1982

Assessment of vasodilator therapy in patients with severe congestive heart failure: limitations of measurements of left ventricular ejection fraction and volumes.

Although noninvasive techniques are often used to assess the effect of vasodilator therapy in patients with congestive heart failure, it is unknown whether changes in noninvasively determined left ventricular ejection fraction, volume, or dimension reliably reflect alterations in intracardiac pressure and flow. Accordingly, we compared the acute effect of sodium nitroprusside on left ventricular volume and ejection fraction (determined scintigraphically) with its effect on intracardiac pressure and forward cardiac index (determined by thermodilution) in 12 patients with severe, chronic congestive heart failure and a markedly dilated left ventricle. Nitroprusside (infused at 1.3 +/- 1.1 [mean +/- standard deviation] microgram/kg/min) caused a decrease in mean systemic arterial, mean pulmonary arterial, and mean pulmonary capillary wedge pressure as well as a concomitant increase in forward cardiac index. Simultaneously, left ventricular end-diastolic and end-systolic volume indexes decreased, but the scintigraphically determined cardiac index did not change significantly. Left ventricular ejection fraction averaged 0.19 +/- 0.05 before nitroprusside administration and increased by less than 0.05 units in response to nitroprusside in 11 of 12 patients. The only significant correlation between scintigraphically and invasively determined variables was that between the percent change in end-diastolic volume index and the percent change in pulmonary capillary wedge pressure (r = 0.68, p = 0.01). Although nitroprusside produced changes in scintigraphically determined left ventricular ejection fraction, end-systolic volume index, and cardiac index, these alterations bore no predictable relation to changes in intracardiac pressure, forward cardiac index, or vascular resistance. Furthermore, nitroprusside produced a considerably greater percent change in the invasively measured variables than in the scintigraphically determined ones.

Blood Pressure↗
PubMed1982

Aortic regurgitation and sinus of Valsalva-right atrial fistula after blunt thoracic trauma.

Non-penetrating chest trauma commonly causes a wide variety of cardiac injuries. Disruption of the aortic valve with resultant aortic regurgitation is not uncommon; conversely, a sinus of Valsalva-right atrial fistula, in the absence of a congenital sinus of Valsalva aneurysm, has been reported only once previously. This report describes the detection by preoperative cardiac catheterisation of both aortic regurgitation, and a sinus of Valsalva-right atrial fistula after blunt chest trauma, and its surgical management. The need for preoperative cardiac catheterisation in patients suffering from non-penetrating cardiac trauma is emphasised, even when the diagnosis appears cleas, because of the diverse nature and possible multiplicity of cardiac lesions.

Adult↗