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Dive into the research topics where Patrick J. Scanlon is active.

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Featured researches published by Patrick J. Scanlon.


Circulation | 1973

Accelerated Angina Pectoris Clinical, Hemodynamic, Arteriographic, and Therapeutic Experience in 85 Patients

Patrick J. Scanlon; Rimgaudas Nemickas; John F. Moran; James V. Talano; Firouz Amirparviz; Roque Pifarre

Eighty-five patients with accelerated (preinfarction) angina are reported. Six suffered acute myocardial infarction awaiting catheterization and coronary angiography, so were not studied. Seventy-nine had coronary arteriography and other angiographic and hemodynamic studies. Fifteen of these 79 patients had normal coronary arteriograms; 64 had significant coronary artery obstruction. The clinical manifestations in 64 abnormal patients did not differ from those with normal arteriograms. Hemodynamic abnormalities correlated with the severity of arteriographic abnormalities. Of 70 patients with coronary artery disease, including the six not studied because of infarction, 48 were treated surgically with a mortality of 12.5%. Mortality for those 22 patients treated without surgery was 27%. Mortality could be correlated with certain risk factors: (1) congestive heart failure; (2) more than three-vessel coronary disease; (3) left ventricular end-diastolic pressure > 12 mm Hg; (4) cardiac index <2.7 liters/min/m2; (5) stroke index <35 ml/beat/m2; (6) estimated cardiac work (mean aortic pressure × cardiac index) <240 units; and (7) ejection fraction <0.50. Cardiac catheterization and angiography were performed without major complications in 97% of patients.


Journal of the American College of Cardiology | 1993

Cardiovascular effects of lightning strikes

Robert C. Lichtenberg; David J. Dries; Kathleen Ward; Wendy Marshall; Patrick J. Scanlon

OBJECTIVESnThe purpose of this study was to investigate the effects of lightning strikes on the cardiovascular system.nnnBACKGROUNDnA lightning strike can attack its victims in one of three ways: direct hit, splash or ground strike. The cardiovascular system can be affected directly by mechanical or electrical trauma during a direct hit or can be indirectly affected through effects on the total body with extensive catecholamine release or autonomic stimulation. Reported effects include hypertension, tachycardia, nonspecific electrocardiographic (ECG) changes including prolongation of the corrected QT (QTc) interval, transient T wave inversion and myocardial necrosis with creatine kinase-MB (CK-MB) fraction release.nnnMETHODSnNineteen victims from five separate lightning strikes were studied over a 2-month period. Each patient was evaluated by serial ECG, CK-MB determinations and echocardiography.nnnRESULTSnThe early (0 to 72 h) effects of lightning were demonstrated on the ECG by ST segment elevation consistent with acute current of injury, prolonged QTc interval with direct hits and nonspecific ST and T wave changes. On echocardiography, segmental or global ventricular dysfunction was seen, and pericardial effusion was also detected. During the intermediate (3- to 14-day) period, new and often marked ECG changes consistent with pericarditis or ischemia were seen. No new echocardiographic changes were detected, however, and the early abnormalities including severe left ventricular dysfunction with cardiogenic shock have reversed. The late (1 to 12 months) period revealed only one patient with long-term sequelae (recurrent pericarditis that persisted for 5 months).nnnCONCLUSIONSnUnless both entrance and exit sites are limited to the lower limbs, direct and splash lightning strikes cause myocardial damage as assessed by abnormal serum enzyme determinations or abnormal echocardiographic findings. Only direct hits resulted in echocardiographic abnormalities or a prolonged QTc interval. The degree of myocardial injury can be severe with left and right ventricular ejection fraction < 15% and can be reversible.


American Heart Journal | 1985

In vivo effects of acute changes in osmolality and sodium concentration on myocardial contractility

Gregory A. Kozeny; David K. Murdock; D.E Euler; Jessie E. Hano; Patrick J. Scanlon; Vinod Bansal; Leonard L. Vertuno

Effects of acute changes in osmolality and sodium concentration (Na) on myocardial contractility (MC) were examined in anesthetized dogs. Using a carotid to left anterior descending bypass, 4 cc of NaCl and/or dextrose of varying osmolality as injected and the percentage of change in MC measured. At Na = O mEq/L, a positive inotropic response occurred, which varied inversely as osmolality increased from 300 (MC = 100 +/- 23%) to 700 mOsm/L (MC = 39 +/- 10%, p less than 0.01). Similar ranges of positive responses of lesser magnitude were noted at Na = 75 mEq/L. At Na = 150, 190, or 350 mEq/L, similar increments in osmolality caused an increasingly negative inotropic response. An inverse relationship between Na and MC was noted with osmolality held constant. Injections of the nonionic contrast agent, P297, in 5% dextrose or 0.9% NaCl, resulted in 28 +/- 3% or -17 +/- 4% (p less than 0.01) change in MC, respectively. Sodium concentration and osmolality have independent effects on MC. Hyperosmolality/hypernatremia causes a negative inotropic response while hyponatremia causes a positive one.


Angiology | 1990

Cardiac Lymphoma Associated with Superior Vena Caval Syndrome and Cardiac Tamponade: Case History

Ming H. Hwang; Alan S. Brown; Zhen En Piao; Patrick J. Scanlon

A sixty-three-year-old patient with malignant histiocytic lymphoma of the heart presented with both superior vena cava syndrome and cardiac tamponade. A two-dimensional echocardiogram showed a large tumor mass in the right atrium and pericardial effusion with right ventricular compression. Superior and inferior vena cavagrams disclosed a lobulated tumor located in the right atrium that extended into and obstructed the superior vena cava. After the pericardial effusion was drained and the diagnosis was established, the patient was irradiated and given chemotherapy with resolution of the tamponade and superior vena cava obstruction.


Progress in Cardiovascular Diseases | 1981

The intermediate coronary syndrome

Patrick J. Scanlon

T HE term “intermediate coronary syndrome” was first used by Graybiel in 1955.’ He defined this syndrome as “an acute attack complicating coronary heart disease in which evaluation of the pain distinguishes it from the angina1 syndrome, and evaluation of the other clinical findings distinguishes it from myocardial infarction.” He was primarily interested in defining a clinical syndrome and not in its “obscure pathophysiologic mechanisms.” Prolonged duration was considered the most important characteristic of the pain of this syndrome to distinguish it from typical angina. Pain arising without obvious cause, such as spontaneous rest pain or pain with mild stress that would ordinarily be easily tolerated by the patient, was another typical feature. During subsequent years, the intermediate coronary syndrome was lumped together with other coronary syndromes, such as preliminary pain,* impending myocardial infarction3 acute coronary insufficiency,4 preinfarction angina,5 and accelerating angina,6 under the umbrella term “unstable angina,“7 in an attempt to develop an acceptable uniform nomenclature. Though unstable angina has become accepted and is now widely used in medical literature, some authors have decried the generality of the term and have attempted to break it down into more precise subgroups.’ The classification that has become most recognized has been that of Conti et a1.,9 who suggested a division of unstable angina into three subgroups. Group I would include patients with angina on effort of recent onset. Group II would be patients with angina on effort whose pattern was changing or progressing. Group III patients would be those who had angina at rest, with pain generally lasting 15 min or more during an episode. This group would include those with rest pain as an initial symptom and those whose rest pain followed an earlier course of stable angina. A high-risk subcategory, which can be designated group IIIa, is made up of those patients whose rest pain is refractory to medical treatment after 24-48 hr of hospitalization. Group III unstable angina closely resembles the intermediate coronary syndrome of Graybiel. For purposes of simplicity, the two will be considered to be the same for this article.


Clinical and Applied Thrombosis-Hemostasis | 1999

Anticoagulant Therapy of Pregnant Patients with Prosthetic Heart Valves : Rationale for a Clinical Trial of Low Molecular Weight Heparin

Harry L. Messmore; Ramesh Kundur; William H. Wehrmacher; Patrick J. Scanlon

The management of anticoagulant therapy for the prevention of thromboembolism from prosthetic heart valves in the pregnant patient is far from ideal and deserves more clinical research. Warfarin therapy given alone throughout pregnancy poses high risks to the fetus because it crosses the placental barrier. Heparin alone throughout pregnancy poses high risks to the mother, which might be lessened somewhat by more inten sive therapeutic regimens and careful monitoring of the heparin level or anticoagulated state of the blood. Because of the major risk of embryopathy in the fetus during the first trimester and latter half of the third trimester, heparin therapy during those times has been recommended. In the opinion of some experts, high-risk cases may benefit from low-dose aspirin in addition to anticoagulant therapy. The fact that warfarin is contraindi cated during pregnancy (according to the pharmaceutical com pany that markets it) poses some problems for the physician who prescribes it. For the above reason, alternative drugs are worthy of consideration and should be given clinical trials. Low molecular weight heparin has the potential for greatly reducing drug-related risk for the fetus while providing greater safety for the mother.


American Heart Journal | 1989

The mechanism and significance of ventricularization of intracoronary pressure during coronary angiography

Ivan Pacold; Ming H. Hwang; Zhen En Piao; Patrick J. Scanlon; Henry S. Loeb

Ventricularization of pressure during coronary angiography has been said to identify the presence of left main coronary artery disease, but the hemodynamic features and the mechanism of this process have not been studied. Twenty consecutive patients with ventricularization were identified prospectively in our laboratory. Four patients had a discrete ostial left main stenosis and 16 patients had stenosis of the entire length of the left main coronary artery. The degree of pressure drop upon cannulation of the diseased left main coronary artery was highly variable; the systolic pressure decreased by 9 to 94 mm Hg, and the diastolic pressure decreased by 6 to 60 mm Hg. The morphology of the ventricularized pressure was distinct. It had a presystolic deflection resembling an a wave. The upstroke of this waveform was slower and the downstroke was steeper than that of the aortic pressure. An identical waveform was observed in dogs after partial occlusion of the left main coronary artery with a balloon-tipped catheter. The waveform of the so-called ventricularized pressure is derived from the aortic pressure, which is altered by its transmission across the left main coronary stenosis. The appearance of ventricularization is an important clue to the presence of left main coronary artery disease.


Journal of the American College of Cardiology | 1995

987-105 Transesophageal Echocardiographic Quantltation of Systolic Mitral Leaflet Displacement In Patients with Mitral Valve Prolapse

David Langholz; William J. Mackin; Diane E. Wallis; William Jacobs; Patrick J. Scanlon; Eric K. Louie

While transesophageal echocardiography (TEE) provides detailed structural information about the mitral valve, the range of normal systolic displacement of the mitral leaflets and the best criteria for diagnosing mitral valve prolapse (MVP) by this technique remain controversial. The area subtended by the systolic displacement of the mitral leaflets into the left atrium beyond the annular hinge points on 4 chamber and 2 chamber images of the mitral valve was measured by TEE in a blinded prospective study of 11 MVP pts (who had systolic displacement of the mitral leaflets superior to the mitral annular plane on parasternal long axis images by transthoracic echo and click and/or late systolic murmur on physical exam) and 11 NORMAL subjects (who had no evidence for MVP by either transthoracic echo or exam). Area Subtended by Systolic Displacement of Mitral Leaflets (cm 2 ) 4 Chamber View 2 Chamber View AMV PMV AMV PMV MVP 0.82xa0±xa00.78 0.40xa0±xa00.43 1.01xa0±xa00.99 0.72xa0±xa00.76 NORMAL 0.03xa0±xa00.06 ** 0.00xa0±xa00.00 ** 0.18xa0±xa00.29 * 0.03xa0±xa00.05 ** Axa0=xa0anterior, Pxa0=xa0posterior, MVxa0=xa0mitral valve ** pxa0lxa00.01 * pxa0lxa00.02 By TEE the area subtended by the superior displacement of the mitral leaflets into the left atrium was significantly greater for MVP pts than for NORMAL subjects. In NORMAL subjects superior displacement of the PMV was never detected in the 4 chamber view, but small degrees of superior displacement were occasionally detected in the 2 chamber view. As many as 6 of 11 NORMAL subjects exhibited minor degrees of superior displacement of the AMV. If an upper limit of normal of 0.5xa0cm 2 is set for the total area subtended by both leaflets in both views, this criterion is 100% sensitive and 82% specific forthe diagnosis of MVP. Conclusions Though TEE demonstrates greater systolic mitral leaflet displacement in MVP than in NORMAl. there is overlap in the range of superior systolic displacement of the mitral valve into the left atrium between MVP pts and NORMAL subjects. The presence of mild superior systolic displacement of the leaflets relative to the annular hinge points by TEE is inadequate to unambiguously identify MVP pts.


Circulation | 1975

Influence of surgery on survival in 145 patients with left main coronary artery disease.

Talano Jv; Patrick J. Scanlon; Meadows Wr; Kahn M; Roque Pifarre; Rolf M. Gunnar


Circulation | 1976

Balloon counterpulsation following surgery for ischemic heart disease.

Patrick J. Scanlon; O'Connell J; Johnson Sa; John M. Moran; Rolf M. Gunnar; Pifarrie R

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Rolf M. Gunnar

Loyola University Chicago

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Henry S. Loeb

Loyola University Chicago

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Ming H. Hwang

Loyola University Chicago

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Ivan Pacold

Loyola University Chicago

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John M. Moran

Loyola University Chicago

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Roque Pifarre

Loyola University Chicago

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Zhen En Piao

Loyola University Chicago

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Alan S. Brown

Advocate Lutheran General Hospital

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Behrooz Eshaghy

Loyola University Chicago

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