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Biomedical subjects

E I Curtiss

Publications and source records attributed to E I Curtiss.

At least 19 recordsLinked to original sources
PubMed1994

Myocardial ischemia after orthotopic liver transplantation.

A hypercoagulable state exists after orthotopic liver transplantation. This hematologic abnormality may predispose patients to coronary thrombosis and unstable angina. The incidence of postoperative myocardial ischemia in such patients is unknown. Suitable electrocardiograms and clinical events of consecutive patients undergoing orthotopic liver transplantation (n = 45) and major intraabdominal surgery (n = 28) during a 3-month period at a major university teaching hospital and transplant center were examined retrospectively. Clinical myocardial ischemia or ischemic electrocardiographic changes, or both, occurred in 6 transplant patients compared with no patient in the nontransplant or comparison group. In 4 of the 6 patients with dramatic electrocardiographic changes and ischemic events, coronary arteriography failed to demonstrate significant obstructive disease. It is concluded that severe myocardial ischemia may occur in patients after orthotopic liver transplantation in the absence of significant coronary disease. A hypercoagulable state may predispose to coronary thrombosis in this setting, providing insight (and a future model for study) into the development of unstable angina.

Abdomen↗
PubMed1991

Changes in left ventricular systolic function that accompany rejection of the transplanted heart: a serial radionuclide assessment of fifty-three consecutive cases.

To examine the functional changes that accompany the development of rejection of the orthotopically transplanted heart, radionuclide ventriculograms, right heart catheterizations, and endomyocardial biopsies were performed at weekly intervals during the posttransplantation hospitalization of 53 consecutive transplant recipients. Left ventricular ejection fraction decreased in those (n = 10) who had sequential biopsies that changed from no rejection to moderate rejection (63% +/- 7% to 57% +/- 7% respectively, p = 0.007). There was an associated decrease in the peak ejection rate (4.4 +/- 1.0 to 3.9 +/- 0.8 end-diastolic volumes per second, p = 0.008) and an increase in the time to peak ejection rate (137 +/- 27 msec to 153 +/- 20 msec, p = 0.004) that accompanied the development of rejection. There was a similar decrease in left ventricular ejection fraction in those (n = 9) who had sequential biopsies that changed from no rejection to mild rejection (63% +/- 6% to 59% +/- 8%, p = 0.009). Only two of 19 patients whose biopsies changed from no rejection to either mild or moderate rejection did not have an associated decrease in ejection fraction. In patients who had a biopsy that showed definite rejection, which was then followed by histologic resolution after treatment (n = 11), left ventricular ejection fraction increased from 56% +/- 8% to 61% +/- 8%, p = 0.03. There were no significant changes in any of the parameters of diastolic function or in any of the hemodynamic parameters measured, which were associated with either the development or resolution of rejection.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Spectrum of hemodynamic changes in cardiac tamponade.

To investigate the pathophysiology of cardiac tamponade, the hemodynamics of 77 consecutive patients with greater than 150 ml of pericardial effusion were studied. Patients were classified into 3 groups based on the equilibration of intrapericardial with right atrial and pulmonary arterial wedge pressures (mm Hg): group I (n = 16), intrapericardial pressure was less than right atrial and pulmonary arterial wedge pressures; group II (n = 13), intrapericardial pressure was equilibrated with right atrial but not pulmonary arterial wedge pressures; group III (n = 48), intrapericardial pressure was equilibrated with right atrial and pulmonary arterial wedge pressures. Pericardiocentesis produced the following changes: group I--significant (p less than 0.03) decreases in intrapericardial pressure (7 +/- 2 mm Hg), right atrial pressure (3 +/- 2 mm Hg), pulmonary arterial wedge pressure (2 +/- 2 mm Hg), and the inspiratory decrease in arterial systolic pressure (3 +/- 4 mm Hg) but no significant change in cardiac output; group II--significant (p less than 0.02) decreases in intrapericardial pressure (11 +/- 5 mm Hg), right atrial pressure (6 +/- 4 mm Hg), pulmonary arterial wedge pressure (4 +/- 5 mm Hg), and inspiratory decrease in arterial systolic pressure (8 +/- 7 mm Hg), and increase in cardiac output (1.1 +/- 1.2 liters/min); group III--significant (p less than 0.001) decreases in intrapericardial pressure (16 +/- 7 mm Hg), right atrial pressure (9 +/- 4 mm Hg), pulmonary arterial wedge pressure (8 +/- 5 mm Hg), inspiratory decrease in arterial systolic pressure (17 +/- 11 mm Hg), and increase in cardiac output (2.8 +/- 1.5 liters/min). The changes after pericardiocentesis in all parameters were significantly (p less than 0.05) greater in group III than in groups I or II except for the change in right atrial pressure, which was not significantly different in groups II versus III. The changes after pericardiocentesis indicate pericardial effusion caused the greatest abnormalities in group III but also caused significant abnormalities of pressure and flow in group II and of pressure alone in group I.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Tamponade↗
PubMed1990

The scalar electrocardiogram of the orthotopic heart transplant recipient.

The 12-lead scalar electrocardiograms of heart transplant recipients were examined prior to hospital discharge (N = 191), and at 1 (N = 162), 2 (N = 97), and 3 years (N = 46) after transplantation. At the pre-discharge point, 46% had right bundle branch block (RBBB) QRS morphology (QRS duration greater than or equal to 120 msec: 20 patients, less than 120 msec: 67 patients). This finding tended to be manifest on the first day following transplantation; its prevalence remained constant over 3 years of follow up. Rejection, ischemic time, preoperative pulmonary vascular resistance, and donor age were not associated with the presence of RBBB morphology. A subgroup of 46 consecutive patients (21 with RBBB morphology) underwent right-sided heart catheterization and radionuclide angiography prior to discharge. RBBB morphology was not associated with any hemodynamic abnormality at catheterization. Based on the radionuclide study, RBBB morphology was associated with a greater left anterior oblique angle required for the best visual separation of the ventricles during acquisition of the study (angle of interventricular septal plane to sagittal plane: 69 +/- 11 versus 59 +/- 9 degrees; p = 0.019), and with the presence of right ventricular dysfunction (13 of 21 versus 6 of 25 patients; p = 0.009). The high prevalence of RBBB morphology in heart transplant recipients appears to be related to posterior rotation of the long axis of the heart in the transverse plane, probably resulting from the surgical technique, and to right ventricular dysfunction.

Adult↗
PubMed1990

Noninvasive evaluation of supraventricular tachycardias.

In this article we discuss the role of noninvasive methods in evaluation of supraventricular tachycardias. The limitation of Holter monitoring and exercise testing is discussed. A significant portion of the article is devoted to the role of esophageal recording, body surface potential mapping, and phase image analysis, areas that are often underutilized but that have potential in the diagnosis of supraventricular tachycardias.

Atrial Flutter↗
PubMed1990

Bradyarrhythmia after heart transplantation. Incidence, time course, and outcome.

From June 1980 to April 1989, 72 of 401 (18%) adult recipients of orthotopic heart transplantation developed prolonged (greater than 24 hours) bradyarrhythmias (less than 60 beats/min) within 5 days after transplantation. Junctional bradycardia occurred in 50 (69%) recipients, sinus bradycardia in 18 (25%), and slow ventricular response during atrial fibrillation in four (6%). Fifty-five of 72 (76%) patients had bradyarrhythmias of less than 20 days' duration (less than 7 days, 50 patients; 7-20 days, five patients). Fifty patients returned to sinus rhythm (greater than 60 beats/min) by the time of discharge. Five patients expired within 20 days. Seventeen of 72 (24%) patients had bradyarrhythmia for more than 20 days, which was symptomatic in 11. All 17 patients (junctional bradycardia, 13 patients; sinus bradycardia, four patients) received a permanent pacemaker within 40 days after transplantation. Between 1 and 12 months (mean, 4 +/- 3 months) after pacemaker implantation, 12 patients recovered sinus rhythm (greater than 70 beats/min). The other five patients had intrinsic rates of 32-57 beats/min (mean, 48 +/- 10 beats/min) during 1-9 months (mean, 4 +/- 3 months) of follow-up. The donor ischemic time in bradyarrhythmia patients was 202 +/- 34 minutes, which was significantly longer (p less than 0.01) than the 173 +/- 43 minutes for those patients without bradyarrhythmia. Conclusively, the incidence of posttransplantation bradyarrhythmia is relatively high. It is usually temporary, however, even in patients with a prolonged duration of bradyarrhythmia. A relation appears to exist between donor ischemic time and the incidence of bradyarrhythmia.

Adult↗
PubMed1990

Cardiac tamponade.

Hemodynamic abnormalities induced by pericardial effusion can be categorized by stages. During phase I, pericardial and left and right ventricular pressures are elevated but not equilibrated, and cardiac output is not compromised. During phase II, elevated pericardial and right ventricular filling pressures are equilibrated with each other but not with left ventricular filling pressure, which is higher. Cardiac output is compromised, and pulsus paradoxus is present in most but not all patients. During phase III, elevated pericardial right ventricular and left ventricular filling pressures are equilibrated, cardiac output is severely compromised, and pulsus paradoxus is present in all patients.

Blood Pressure↗
PubMed1990

The duration of Holter monitoring in patients with syncope. Is 24 hours enough?

To determine the incremental yield of ambulatory monitoring in the evaluation of syncope, three serial 24-hour Holter recordings were obtained in a consecutive series of 95 patients with syncope, the cause of which was not explained by history, physical examination, or 12-lead electrocardiogram. The mean age of patients was 61 years and 41% were men. Major electrocardiographic abnormalities were found in 26 patients (27%), including unsustained ventricular tachycardia (19 patients), pauses of at least 2 seconds (8 patients), profound bradycardia (1 patient), and complete heart block (1 patient). The first 24-hour Holter recording had at least one major abnormality in 14 patients (15%) (95% confidence interval, 8.3% to 23.4%). Of the 81 patients without a major abnormality on the first Holter recording, the second Holter recording had major abnormalities in 9 (11%) (95% confidence interval, 5.1% to 20.0%). Of the 72 patients without a major abnormality on the first two Holter recordings, only 3 patients (4.2%) had a major abnormality on the third Holter recording (95% confidence interval, 0.8% to 11.7%). Four factors were significantly associated with an increased likelihood of a major abnormality on 72 hours of monitoring: age above 65 years (relative risk, 2.2), male gender (relative risk, 2.0), history of heart disease (relative risk, 2.2), and an initial nonsinus rhythm (relative risk, 3.5). These results suggest that 24 hours of Holter monitoring is not enough to identify all potentially important arrhythmias in patients with syncope. Monitoring may need to be extended to 48 hours if the first 24-hour Holter recording is normal.

Adolescent↗
PubMed1990

A controlled clinicopathologic study of myocardial fibrosis in systemic sclerosis (scleroderma).

Clinicopathologic correlations of myocardial fibrosis were examined in 54 autopsied patients with scleroderma and 54 age and sex matched autopsy controls. Thirty eight (70%) of the patients with scleroderma had myocardial fibrosis compared to 20 (37%) of the controls (p less than 0.005). There was no significant difference in the prevalence of contraction band necrosis in the patients with scleroderma (22%) compared to controls (17%). Patients with scleroderma with left ventricular dysfunction in the absence of other causative factors clinically had a greater prevalence of both advanced myocardial fibrosis (60%) and contraction band necrosis (40%) than did the other patients with scleroderma or the controls. We conclude that patients with scleroderma with the greatest likelihood of advanced myocardial fibrosis can be identified clinically, and their findings are consistent with the presence of microvascular coronary vasospasm, a "myocardial Raynaud's phenomenon."

Adult↗
PubMed1988

Pulsus paradoxus: definition and relation to the severity of cardiac tamponade.

Based on 101 control patients, the 95% confidence limit for the inspiratory decrease in arterial systolic pressure (delta SYST, mm Hg) and the percentage decrease in arterial systolic pressure (% delta SYST = delta SYST/expiratory systolic pressure) were determined to be 12 mm Hg and 9%, respectively. In 65 patients with pericardial effusion, the severity of cardiac tamponade was estimated on the basis of the percentage increase in cardiac output resulting from pericardiocentesis: absent = less than 20% (n = 24), mild = 20% to 49% (n = 9), and moderate or severe = greater than or equal to 50% (n = 32). The accuracy of a delta SYST greater than 12 mm Hg and % delta SYST greater than 9% in the identification of tamponade was 92% and 97%, respectively. A % delta SYST greater than 15% with relative hypotension (expiratory systolic pressure less than or equal to 120 mm Hg) or a delta SYST greater than 25 mm Hg or inspiratory pulse obliteration was found in 31 of 32 patients with moderate or severe tamponade compared to 2 of the 33 remaining patients. We conclude that the inspiratory decline in arterial systolic pressure can be used to accurately estimate the level of hemodynamic embarrassment resulting from pericardial effusion.

Blood Pressure↗
PubMed1987

Electrocardiographically discrete right and left ventricular QRS complexes: a case report.

A patient with congestive cardiomyopathy manifested a right ventricular QRS followed after 80 msec. by a left ventricular QRS in response to a single atrial depolarization. The ventricular sequence was reversible when the left ventricle was paced directly. Virtually the entire ipsilateral ventricular ejection period occurred during diastolic filling of the contralateral ventricle. Triggered left ventricular pacing, using the right ventricular electrogram as trigger, shortened the QRSRV-QRSLV interval and resulted in a reduction of left ventricular filling pressure and a significant rise in cardiac output. These findings indicated an independent contribution of this unique form of interventricular conduction disturbance to deterioration in hemodynamic performance.

Atrial Flutter↗
PubMed1985

The electrocardiogram in systemic sclerosis (scleroderma). Study of 102 consecutive cases with functional correlations and review of the literature.

The electrocardiographic findings in 102 consecutive patients with scleroderma were reviewed to determine the frequency and nature of the electrocardiographic abnormalities associated with this disease. Septal infarction pattern unassociated with QRS prolongation was present in 10 percent, compared with none of 96 control subjects (p less than 0.001). Ventricular conduction abnormalities were present in 17 percent. A normal electrocardiogram was obtained in 49 percent. A subset of 48 patients underwent detailed cardiopulmonary evaluation including exercise thallium scintigraphy, rest and exercise radionuclide ventriculography, pulmonary function tests, and chest roentgenography. Functional correlations of the electrocardiographic findings were examined in this subset. Septal infarction pattern (five of 48) and ventricular conduction abnormalities (10 of 48) were both associated with septal or anteroseptal thallium perfusion abnormalities (10 of 15 versus six of 33 of the remainder, p less than 0.005), which were present despite normal coronary angiographic results. Thallium defect scores were greater in patients with septal infarction pattern or ventricular conduction abnormalities compared with the remainder (defect scores 3.0 +/- 2.6 versus 1.4 +/- 2.2, respectively, p less than 0.025). In patients with ventricular conduction abnormalities, both left bundle branch block and right bundle branch block with left anterior fascicular block were associated with abnormal left ventricular function, whereas isolated right bundle branch block or left anterior fascicular block was associated with normal left ventricular function. A normal electrocardiographic finding (19 of 48) was associated with normal left ventricular function at rest (19 of 19). However, 11 of 19 (58 percent) had thallium perfusion defects and four of 19 (21 percent) had an abnormal response to exercise, although in none was the peak ejection fraction less than 50 percent. It is concluded that both septal infarction pattern and ventricular conduction abnormalities are electrocardiographic abnormalities associated with scleroderma heart disease; they appear to be a result of myocardial fibrosis. Some degree of myocardial fibrosis may be present with a normal electrocardiographic result, but significant left ventricular dysfunction is unlikely. Septal infarction pattern and ventricular conduction abnormalities, when present, are indicators of more advanced fibrosis.

Adult↗
PubMed1984

Intermittent mitral regurgitation due to Beall valve dysfunction: analysis of 13 patients with atrial fibrillation.

A unique hemodynamic event was noted in long-term survivors of mitral valve replacement with the Beall prosthesis. The event was a result of intermittent valve dysfunction and transvalvular mitral regurgitation (MR). At cycle lengths longer than 0.9 second that were preceded by shorter cycle lengths, 8 of 13 patients with Beall valve prostheses who had chronic atrial fibrillation (AF) intermittently had a marked unexpected decrease in peak left ventricular systolic pressure and a simultaneous increase in left atrial or pulmonary artery wedge "v" wave pressure. This event, which is a result of intermittent, severe MR, occurred more frequently at longer cycle lengths. In all 8 patients with the finding, severe valve disc wear was found at operation; however, 5 of these patients had only trace or 1+ MR on left ventricular angiography. In contrast, the event did not occur in 11 patients in chronic AF with organic MR or non-Beall valve MR, despite an appropriate number of sufficiently long cycles. The absence of the event in 5 Beall valve patients with significantly faster heart rates than in those with the event may in part be a result of its dependence on cycle length. This hemodynamic event, when present in a Beall valve recipient in AF, is an indication for valve replacement, even in the absence of angiographic evidence of severe MR.

Atrial Fibrillation↗
PubMed1984

Physiologic abnormalities of cardiac function in progressive systemic sclerosis with diffuse scleroderma.

To investigate cardiopulmonary function in progressive systemic sclerosis with diffuse scleroderma, we studied 26 patients with maximal exercise and redistribution thallium scans, rest and exercise radionuclide ventriculography, pulmonary-function testing, and chest roentgenography. Although only 6 patients had clinical evidence of cardiac involvement, 20 had abnormal thallium scans, including 10 with reversible exercise-induced defects and 18 with fixed defects (8 had both). Seven of the 10 patients who had exercise-induced defects and underwent cardiac catheterization had normal coronary angiograms. Mean resting left ventricular ejection fraction and mean resting right ventricular ejection fraction were lower in patients with post-exercise left ventricular thallium defect scores above the median (59 +/- 13 per cent vs. 69 +/- 6 per cent [P less than 0.025], and 36 +/- 12 per cent vs. 47 +/- 7 per cent [P less than 0.025], respectively). We conclude that in progressive systemic sclerosis with diffuse scleroderma, abnormalities of myocardial perfusion are common and appear to be due to a disturbance of the myocardial microcirculation. Both right and left ventricular dysfunction appear to be related to this circulatory disturbance, suggesting ischemically mediated injury.

Adult↗
PubMed1984

Myocardial function and perfusion in the CREST syndrome variant of progressive systemic sclerosis. Exercise radionuclide evaluation and comparison with diffuse scleroderma.

Myocardial function and perfusion were evaluated in 22 patients with progressive systemic sclerosis with the CREST syndrome using exercise and radionuclide techniques, pulmonary function testing, and chest roentgenography. The results were compared with a similar study of 26 patients with progressive systemic sclerosis with diffuse scleroderma. The prevalence of thallium perfusion abnormalities was similar in the groups with CREST syndrome and diffuse scleroderma, (64 percent versus 77 percent), but the defects were significantly smaller in the CREST syndrome (p less than 0.01). Reperfusion thallium defects in the absence of extramural coronary artery disease were seen in 38 percent of patients with diffuse scleroderma. This finding was not seen in any of the patients with the CREST syndrome. In diffuse scleroderma, abnormalities of both right and left ventricular function were related to larger thallium perfusion defects. In the CREST syndrome, abnormalities of left ventricular function were minor, were seen only during exercise, and were unrelated to thallium perfusion defects. Abnormal resting right ventricular function was seen in 36 percent of the patients with the CREST syndrome and was associated with an isolated decrease in diffusing capacity of carbon monoxide. It is concluded that the cardiac manifestations of the CREST syndrome are distinct from those found in diffuse scleroderma. Unlike diffuse scleroderma, abnormalities of left ventricular function in the CREST syndrome are minor and are unrelated to abnormalities of coronary perfusion. Right ventricular dysfunction in the CREST syndrome appears to be primarily related to pulmonary vascular disease.

Adult↗