Search PubMed⌕ Search

Biomedical subjects

B Pitt

Publications and source records attributed to B Pitt.

At least 199 records · Page 11Linked to original sources

Safety of helicopter transport and out-of-hospital intravenous fibrinolytic therapy in patients with evolving myocardial infarction.

Of 150 consecutive patients with acute myocardial infarction transported by helicopter for acute intervention, 55 had intravenous thrombolytic therapy (tissue plasminogen activator in 12, streptokinase in 43) initiated prior to transfer. Patients were transported 55 +/- 10 ground miles in 17 +/- 6 minutes and no patient died or experienced bleeding or hemodynamic instability during transfer. Patients receiving thrombolytic therapy had a higher incidence of arrhythmias during transit compared to the untreated group, ventricular tachycardia in six and third-degree atrioventricular block in one compared to ventricular tachycardia in one patient, respectively (p = 0.005). However, these arrhythmias were transient and did not require cardioversion, temporary pacing, or further antiarrhythmic medical treatment. Chest pain was relieved or decreased more frequently in the patients receiving thrombolytic therapy vs. those untreated; 21 of 55 vs. 21 of 95 respectively (p = 0.04). Immediate coronary angiography confirmed a higher incidence and more complete infarct vessel patency (34/55 vs. 30/95) in the patients receiving tissue plasminogen activator or streptokinase (p less than 0.001). Thus, helicopter transfer of patients with evolving myocardial infarction is safe, and early initiation of thrombolytic therapy is associated with increased infarct vessel patency and benign reperfusion arrhythmias.

Aircraft↗

omega-123I-hexadecanoic acid metabolic probe of cardiomyopathy.

The utility of omega-123I-hexadecanoic acid myocardial scintigraphy as a metabolic probe of cardiomyopathies was investigated. Sixteen patients with a variety of cardiomyopathies and myopathies that involve cardiac muscle and ten volunteers were imaged in the postabsorptive state in a 40 degrees LAO projection after a standard dose of omega-123I-hexadecanoic acid. An elimination T1/2 was calculated from the left ventricular myocardial time-activity curve. An uptake index, corrected for chest wall attenuation, was also computed in 7 of 10 volunteers and 8 of 16 patients. Of the 16 patients, only 2 had distinctly abnormal omega-123I-hexadecanoic acid myocardial tracer kinetics. The first patient had a metabolic disorder of which carnitine deficiency was one component. The second patient had endocardial fibroelastosis, a process which has been linked to disorders which deprive the myocardium of oxygen and energy. Therefore, the cardiomyopathy may have been caused by some abnormality of cardiac metabolism other than carnitine deficiency. Although of limited utility in the overall cardiomyopathic population, omega-123I-hexadecanoic acid myocardial scintigraphy should be further investigated as a screening test for carnitine deficiency and related metabolic abnormalities in patients at risk.

Adolescent↗

Long-term follow-up of patients with previous myocarditis using radionuclide ventriculography.

A prospective long-term follow-up study is reported of 18 of 19 patients who survived a bout of presumed myocarditis 6-136 months (average 54 months) previously. The study included 14 males and four females, ranging from 27 to 63 years of age (mean, 44 years). Chest X-ray, ECG, echocardiogram, and resting and exercise radionuclide ventricular ejection fraction (RNVEF) for assessment of ventricular function were evaluated at follow-up. Resting and exercise RNVEF from seven control subjects were evaluated for comparison. Residual abnormalities were noted in chest X-ray (16%), echocardiogram (30%), and ECG (55%) in these predominantly asymptomatic patients (17/18 or 95%). The resting RNVEF (mean +/- SD) for the myocarditis group versus controls were 0.57 +/- 0.1 and 0.65 +/- 0.1 (P = NS), respectively. The exercise RNVED for the myocarditis group versus controls were 0.56 +/- 0.1 and 0.74 +/- 0.05 (P less than 0.01), respectively. Abnormal resting RNVEF was noted in six (33%) and exercise RNVEF in 14 (77%) patients in the myocarditis group. Two patients with abnormal exercise RNVEF subsequently developed findings consistent with dilated cardiomyopathy. It is unclear as to whether the abnormal ventricular function may serve as a marker for future development of dilated cardiomyopathy.

Adult↗

Assessment of dysfunction in aortic regurgitation by stress-shortening relationship.

Some patients with aortic regurgitation develop irreversible left ventricular dysfunction. The purpose of this study was to noninvasively examine left ventricular function in patients with aortic regurgitation by determining the end-systolic stress-shortening relationship using M-mode echocardiography. Ten normal volunteers and 10 patients with chronic, isolated aortic regurgitation were studied at rest and following load and inotropic alteration by cold pressor testing. The baseline ejection phase indices of ejection fraction and percent fractional shortening did not distinguish between normals and patients with aortic regurgitation (74.6% +/- 2.8% versus 67.0% +/- 4.2%, P = NS and 37.6% +/- 2.4% versus 31.6% +/- 2.7%, P = NS, respectively.) End-systolic stress was significantly greater in patients with aortic regurgitation both at rest (107.8 +/- 11.6 dynes/cm2 X 10(-3) versus 68.4 +/- 4.8 dynes/cm2 X 10(-3), P less than 0.005) and after cold pressor intervention (122.8 +/- 13.0 dynes/cm2 X 10(-3) versus 80.1 +/- 4.0 dynes/cm2 X 10(-3), P less than 0.005). Normals showed increased fractional shortening in the presence of increasing end-systolic stress. Patients with aortic regurgitation showed decreased fractional shortening during increased stress. This response suggests either left ventricular dysfunction with increasing stress or decreased myocardial contractile reserve after cold pressor inotropic stimulation. End-systolic stress-percent fractional shortening relationship may be a sensitive indicator of early left ventricular dysfunction in patients with aortic regurgitation.

Aortic Valve Insufficiency↗

Chronic alpha-adrenoceptor blockade with trimazosin in congestive heart failure.

We evaluated chronic adjunctive alpha-1 receptor blockade with trimazosin in congestive heart failure. This agent produced hemodynamic effects consistent with venodilation (reduced left ventricular volume and filling pressure with increased left ventricular ejection fraction), but only during exercise. Resting hemodynamic parameters and exercise duration were not significantly altered by chronic alpha-1 receptor blockade.

Chronic Disease↗

Scintigraphic characterization of amyloid cardiomyopathy.

Amyloidosis is an important entity in the differential diagnosis of cardiac failure of undetermined etiology. In this case report, the typical pattern of combined systolic and diastolic impairment in amyloid cardiomyopathy was demonstrated by analysis of the cardiac blood pool study. In addition, the patient described had mild uptake of Ga-67 citrate, as well as the characteristically intense myocardial uptake of Tc-99m pyrophosphate. Scintigraphic assessment may be particularly helpful when the diagnosis of amyloidosis is being considered in a patient with unexplained cardiac failure.

Aged↗

The independent effects of oxygen radical scavengers on canine infarct size. Reduction by superoxide dismutase but not catalase.

Previous studies demonstrated a significant reduction of ultimate infarct size in the canine heart by the combined administration of superoxide dismutase plus catalase. This study was performed to assess the independent effects of each enzyme on ultimate infarct size due to ischemia/reperfusion. Dogs received 2-hour infusions of superoxide dismutase, catalase, or albumin (controls) via the left atrium beginning 15 minutes before and ending 15 minutes after a 90-minute occlusion of the left circumflex coronary artery. The dogs were killed 6 hours after reperfusion. After histochemical staining, infarct and risk area masses were calculated by gravimetric and planimetric analysis. Infarct size expressed as a percentage of the area at risk was: superoxide dismutase, 19 +/- 5; catalase, 30 +/- 5; and controls, 40 +/- 3. Infarct size in the superoxide dismutase group, but not the catalase group, was significantly less than in controls (P less than 0.05). No significant differences in hemodynamics or area at risk were observed that could explain the differences in infarct size. The results indicate that superoxide dismutase alone protects reperfused ischemic myocardium as well as does the combination of superoxide dismutase and catalase. The beneficial effect of superoxide dismutase and insignificant effect of catalase suggest that tissue damage during ischemia and reperfusion may be mediated largely by superoxide anion but not by hydrogen peroxide.

Animals↗

Assessment of potentially salvageable myocardium during acute myocardial infarction: use of postextrasystolic potentiation.

Twenty-three patients with evolving acute myocardial infarction (AMI) undergoing catheterization for thrombolytic therapy had interventional contrast ventriculography using programmed atrial stimulation. Postextrasystolic (PES) potentiation was present in 67% of infarct-related segments up to 9 hours after the onset of AMI. The presence of segmental potentiation was not related to time from onset of pain to ventriculography, initial ejection fraction, presence of collaterals, left ventricular end-diastolic pressure or the PES delay. In 18 patients reperfusion was successful using intracoronary streptokinase an average of 6.2 hours after the onset of AMI; in these patients repeat contrast ventriculography was performed an average of 11 days after AMI. Improved chronic segmental ventricular function was predicted by the presence of collaterals to the infarct-related artery at the time of acute catheterization (p = 0.02), but was best predicted by analysis of acute PES potentiation (p less than 0.0001). The predictive value of PES analysis was highest in segments without collaterals. Thus, atrial stimulation is safe during AMI and analysis of segmental ventricular function shows potentially viable myocardium up to 9 hours after the onset of AMI. In addition, analysis of PES segmental function can predict chronic function if reperfusion is successful, especially in segments without collaterals. PES ventriculographic analysis may allow prospective determination of which patients during AMI are most likely to benefit from acute thrombolytic therapy.

Aged↗

Effect of OKY-1581, a thromboxane synthetase inhibitor, on coronary thrombosis in the conscious dog.

OKY-1581, a new thromboxane synthetase inhibitor, was studied in a conscious canine model of coronary thrombosis. After thoracotomy with placement of a left circumflex coronary artery flow probe and implantation of an electrode into the circumflex artery, animals were assigned randomly to the following groups: 0.9% NaCl vehicle control or OKY-1581 1 mg/kg every 4 intravenously for 24 h. During the drug treatment period, a 50 microA anodal current was passed through the circumflex electrode, and venous blood was obtained for platelet aggregation studies. As compared to control animals, the OKY-1581 treated animals developed a greater mean coronary flow at the end of the treatment period, smaller thrombi by wet weight, smaller infarcts, and fewer ventricular arrhythmias. Ex vivo platelet aggregation studies revealed significant inhibition of aggregation to standard aggregating agents for the drug treated group only. OKY-1581 is an effective antithrombotic agent which maintains coronary flow after a thrombogenic stimulus, presumably via blockade of the synthesis of thromboxane by blood platelets.

Acrylates↗

Beneficial effects of nafazatrom on ischemic reperfused myocardium.

The effect of nafazatrom, a new antithrombotic agent, was studied in a canine model of regional myocardial ischemia. Nafazatrom was administered 1 mg/kg intravenously every 6 h for 48 h. After 24 h of drug or placebo administration, animals underwent 90 min of occlusion of the proximal left circumflex coronary artery followed by gradual reperfusion over a period of 30 min. Twenty-four hours later, the animals were sacrificed and infarct size was determined by histochemical staining with triphenyltetrazolium chloride. Nafazatrom-treated animals had a significant reduction in infarct size expressed as a percent of the anatomical area at risk for infarction: 21 +/- 5% in the treated group vs. 41 +/- 5% in the control group (X +/- S.E.M., P less than 0.05). Histological examination confirmed the gross results of postmortem histochemical staining. Salvage of ischemically jeopardized tissue appeared to be unrelated to myocardial oxygen demand as there were no hemodynamic differences between groups. The beneficial effects of nafazatrom are presumably related to a limitation of autolytic processes on the heart during and after ischemia as a result of the drug's ability to inhibit lipoxygenase and to prevent the enzymatic degradation of prostacyclin.

Animals↗

Measurement of left ventricular ejection fraction in pediatric patients using the nuclear stethoscope.

Left ventricular (LV) ejection fraction (EF) was measured in 25 patients, aged 2 weeks to 20 years (mean 8.6 years), using a portable nonimaging scintillation stethoscope. Technically satisfactory studies were obtained in 23 patients. LVEF was validated by cineangiography in 19 patients and by standard gated blood pool scintigraphy in 4. EF measured by the nuclear stethoscope correlated well with values obtained by cineangiography or scintigraphy (r = 0.869, p less than 0.001) over a wide range of EF values (18 to 79%). In children younger than 5 years (n = 11), the correlation (r = 0.728, p less than 0.02) was less satisfactory than in those older than 5 years (r = 0.926; p less than 0.001). Although modifications in the instrument and further clinical trials with the stethoscope are needed before the device becomes clinically useful to pediatric cardiologists, our data indicate that the nuclear stethoscope can provide reliable assessment of LVEF in pediatric patients.

Adolescent↗

The exercise response in idiopathic dilated cardiomyopathy.

In order to more clearly define the exercise response of idiopathic dilated cardiomyopathy (IDC), 20 patients in this study with strictly defined IDC were evaluated with radionuclide ventriculography and invasive hemodynamic monitoring. Severe cardiovascular impairment was present at rest, and peak supine exercise produced progressive left ventricular (LV) dilatation in both diastole and systole (mean +/- SEM from 172 +/- 14 to 212 +/- 22 ml/m2 at end-diastole and from 137 +/- 14 to 170 +/- 22 ml/m2 at end-systole; both p less than 0.03). There were marked increases in LV and right ventricular filling pressure (from 17 +/- 2 to 36 +/- 3 mmHg and from 7 +/- 2 to 15 +/- 2 mmHg, respectively; both p less than 0.0001) and increased pulmonary artery pressure. Mean LV ejection fraction did not change significantly with exercise (22 +/- 2 to 23 +/- 3%; p greater than 0.8), but individual patients demonstrated substantial variability. Cardiac output rose less than in normals and increases were brought about primarily by subnormal heart rate increases. High resting and exercise systemic and pulmonary vascular resistance were indicative of limited vasodilator reserve. Despite marked hemodynamic abnormalities, 10 of the 20 subjects had well preserved exercise capacity (greater than or equal to 12 min exercise duration). These patients as a group had significantly lower resting heart rate and higher exercise cardiac output and lower exercise systemic vascular resistance. However, they did not differ from the other patients with respect to resting LV function.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

The effect of dobutamine on exercise performance in patients with symptomatic ischemic heart disease.

The effect of dobutamine on exercise performance was assessed in 20 patients with ischemic heart disease (CAD) and a positive stress test. These patients had a wide range of resting left ventricular ejection fraction (range 22% to 69%, mean 42%). Each patient entered a double-blind crossover study in which two identical exercise radionuclide ventriculograms were performed in patients on dobutamine, 5 micrograms/kg/min intravenously, or placebo. Dobutamine increased resting left ventricular ejection fraction. Although ejection fraction fell with dobutamine during submaximal exercise, it remained higher than with placebo. At peak exercise, ejection fraction fell to the same level on dobutamine as with placebo. Dobutamine diminished exercise time and time to ischemia while peak pressure-rate product was unchanged. Four of 20 patients developed complex ventricular premature beats, all while on dobutamine. Although useful when administered to resting patients with acute left ventricular failure, dobutamine's effects may be deleterious in exercising patients with chronic ischemic heart disease.

Adult↗

Antidysrhythmic actions of meobentine sulfate.

The antiarrhythmic efficacy of meobentine sulfate, a bethanidine derivative lacking inhibitory effects on adrenergic neuronal function, was assessed in three canine models. Intravenous meobentine sulfate, administered in dosages of 5.0, 10,0, and 20.0 mg/kg, produced a dose-related increase in the ventricular fibrillation threshold (VFT) under nonischemic conditions (7.6 +/- 1.8 mA vs 37.8 +/- 8.6 mA) (20 mg/kg; p less than 0.05) and during regional myocardial ischemia (5.6 +/- 1.5 mA vs 41.8 +/- 9.1 mA) (20 mg/kg; p less than 0.05). The VFT was also increased in the presence of chronic ischemic injury (6.4 +/- 1 mA to 31 +/- 10 mA) (20 mg/kg; p 0.05). In the conscious dog, 4 days after an anterior myocardial infarction, programmed electrical stimulation (PES) produced nonsustained ventricular tachycardia (VT) in five dogs. After meobentine sulfate administration, eight of nine animals had sustained VT and one animal developed ventricular fibrillation (VF). At a dose of 20 mg/kg, there was prolongation of the cycle length of the VT (169 +/- 11 msec to 237 +/- 20 msec), prolongation of the QRS duration (58 +/- 2.6 msec to 71 +/- 3.7 msec), and prolongation of the delay in epicardial activation. There was an enhanced potential after meobentine administration for programmed stimulation to produce ventricular arrhythmias with the introduction of fewer premature impulses. In the third canine model, conscious dogs with a previous anterior myocardial infarction developed VF in response to electrically induced left circumflex coronary artery injury. Meobentine (20 mg/kg) failed to prevent VF in eight of eight dogs. These results suggest that while meobentine sulfate significantly increases the electrical VFT, it does not protect the conscious canine from the induction of ventricular tachyarrhythmias in response to PES, and it does not prevent VF in a conscious canine model of sudden coronary death.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗