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Dive into the research topics where Charles H. Croft is active.

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Featured researches published by Charles H. Croft.


American Journal of Cardiology | 1984

Risk factors for sudden death after acute myocardial infarction: Two-year follow-up☆

Jhulan Mukharji; Robert E. Rude; W.Kenneth Poole; Nancy Gustafson; Lewis J. Thomas; H.William Strauss; Allan S Jaffe; James E. Muller; Robert Roberts; Daniel S. Raabe; Charles H. Croft; Eugene Passamani; Eugene Braunwald; James T. Willerson

The risk of sudden coronary death after myocardial infarction (MI) was assessed in 533 patients who survived 10 days after MI and were followed for up to 24 months (mean 18) in the Multicenter Investigation of the Limitation of Infarct Size. Analysis of multiple clinical and laboratory variables determined before hospital discharge revealed that frequent ventricular premature beats (VPBs) (greater than or equal to 10/hour) on ambulatory electrocardiographic monitoring and left ventricular (LV) dysfunction (radionuclide LV ejection fraction less than or equal to 0.40) were independently significant markers of risk for subsequent sudden death believed to be the result of a primary ventricular arrhythmia. The incidence of sudden death was 18% in patients with both LV dysfunction and frequent VPBs (11 times that of patients with neither of these findings). Seventy-nine percent of all sudden deaths occurred within 7 months after the index MI. In 280 survivors reclassified 6 months after MI with regard to the presence or absence of frequent VPBs and LV dysfunction, these risk factors could not be associated with sudden coronary death over a further follow-up period of up to 18 months; the overall incidence of sudden cardiac death was low (1.4%) after 6 months. Thus, the presence of frequent VPBs in association with LV dysfunction early after MI identifies patients at high risk for sudden death over the next 7 months.


American Journal of Cardiology | 1982

Detection of acute right ventricular infarction by right precordial electrocardiography

Charles H. Croft; Pascal Nicod; James R. Corbett; Samuel E. Lewis; Robert Huxley; Jhulan Mukharji; James T. Willerson; Robert E. Rude

The value of 0.1 mV or greater of S-T segment elevation in at least one right precordial lead (V4R to V6R) in defining right ventricular myocardial infarction was assessed prospectively in 43 subjects (33 consecutive patients with enzymatically confirmed infarction of varying type and location, 4 patients with unstable angina and 6 healthy volunteers). Patients with acute myocardial infarction were studied with radionuclide ventriculography and technetium-99m stannous pyrophosphate myocardial scintigraphy 18.2 +/- 14.3 (mean +/- standard deviation) and 85.1 +/- 18.0 hours after the onset of symptoms, respectively. Eleven patients (Group A: 9 patients with transmural inferior infarction, 1 with transmural inferolateral infarction and 1 with transmural anteroseptal infarction) demonstrated right precordial S-T segment elevation and 22 patients (Group B: 6 patients with transmural inferior infarction, 2 with transmural posterior infarction, 3 with transmural inferolateral infarction, 3 with transmural anteroseptal infarction, 3 with transmural extensive anterior infarction, 4 with subendocardial anterior infarction and 1 with unclassified infarction) did not. Right ventricular ejection fraction was significantly lower in Group A (0.47 +/- 0.11) than in Group B (0.60 +/- 0.12) (p less than 0.01). Right ventricular total wall motion score was 63.8 +/- 15.6 percent of normal in Group A versus 94.3 +/- 8.5 percent in Group B (p less than 0.001). Technetium-99m pyrophosphate uptake (2+ or greater) over the right ventricle occurred in nine patients (81.8 percent) in Group A and in one patient (4.5 percent) in Group B (p less than 0.001). No patient with unstable angina and no healthy volunteer had S-T segment elevation in a right precordial lead. S-T segment elevation of 0.1 mV or greater in one or more of leads V4R to V6R is both highly sensitive (90 percent) and specific (91 percent) in identifying acute right ventricular infarction.


American Journal of Cardiology | 1986

Sudden death and its relation to QT-interval prolongation after acute myocardial infarction: Two-year follow-up

Kevin Wheelan; Jhulan Mukharji; Robert E. Rude; W. Kenneth Poole; Nancy Gustafson; Lewis J. Thomas; H. William Strauss; Allan S. Jaffe; James E. Muller; Robert Roberts; Charles H. Croft; Eugene R. Passamani; James T. Willerson

Risk of sudden death was assessed in 533 patients who survived 10 days after acute myocardial infarction (AMI) and were followed for up to 24 months (mean 18) in the Multicenter Investigation of the Limitation of Infarct Size. Analysis of clinical and laboratory variables measured before hospital discharge revealed that the QT interval, either corrected (QTc) or uncorrected for heart rate, did not contribute significantly to prediction of subsequent sudden death or total mortality. In this population, frequent ventricular premature complexes (more than 10 per hour) on ambulatory electrocardiographic monitoring and left ventricular (LV) dysfunction (radionuclide LV ejection fraction of 0.40 or less) identify patients at high risk of sudden death. In patients with these adverse clinical findings, the QTc was 0.468 +/- 0.044 second among those who died suddenly and 0.446 +/- 0.032 second in survivors, and was not statistically significant as an additional predictor of sudden death. Consideration of the use of type I antiarrhythmic agents, digoxin, presence of U waves and correction for intraventricular conduction delay did not alter these findings. Although QT-interval prolongation occurs in some patients after acute myocardial infarction, reduced LV ejection fraction and frequent ventricular premature complexes are the most important factors for predicting subsequent sudden death in this patient population.


Journal of the American College of Cardiology | 1984

Is anterior ST depression with acute transmural inferior infarction due to posterior infarction?: A vectorcardiographic and scintigraphic study

Jhulan Mukharji; Suzanne Murray; Samuel E. Lewis; Charles H. Croft; James R. Corbett; James T. Willerson; Robert E. Rude

The hypothesis that anterior ST segment depression represents concomitant posterior infarction was tested in 49 patients admitted with a first transmural inferior myocardial infarction. Anterior ST depression was defined as 0.1 mV or more ST depression in leads V1, V2 or V3 on an electrocardiogram recorded within 18 hours of infarction. Serial vectorcardiograms and technetium pyrophosphate scans were obtained. Eighty percent of the patients (39 of 49) had anterior ST depression. Of these 39 patients, 34% fulfilled vectorcardiographic criteria for posterior infarction, and 60% had pyrophosphate scanning evidence of posterior infarction. Early anterior ST depression was neither highly sensitive (84%) nor specific (20%) for the detection of posterior infarction as defined by pyrophosphate imaging. Of patients with persistent anterior ST depression (greater than 72 hours), 87% had posterior infarction detected by pyrophosphate scan. In patients with inferior myocardial infarction, vectorcardiographic evidence of posterior infarction correlated poorly with pyrophosphate imaging data. Right ventricular infarction was present on pyrophosphate imaging in 40% of patients with pyrophosphate changes of posterior infarction but without vectorcardiographic evidence of posterior infarction. It is concluded that: 1) the majority of patients with acute inferior myocardial infarction have anterior ST segment depression; 2) early anterior ST segment depression in such patients is not a specific marker for posterior infarction; and 3) standard vectorcardiographic criteria for transmural posterior infarction may be inaccurate in patients with concomitant transmural inferior myocardial infarction or right ventricular infarction, or both.


Journal of the American College of Cardiology | 1985

Modified technique of transseptal left heart catheterization

Charles H. Croft; Kirk Lipscomb

Transseptal left heart catheterization was performed in 106 instances in 101 patients using right anterior oblique fluoroscopy to define septal boundaries during interatrial septal puncture, and using a preshaped guide wire to catheterize the left ventricle. By using these two modifications of the classic transseptal technique, the left atrium was entered in 105 instances (99%) and the left ventricle was catheterized in all 87 attempts (100%), including attempts in eight patients with mitral stenosis (valve area 1.29 +/- 0.39 cm2 [mean +/- standard deviation] ). No deaths occurred as a direct result of transseptal catheterization; nonfatal complications occurred in 2.8% of patients (hemopericardium in one patient, ventricular fibrillation in one patient and transient vagal reaction in one patient). The use of the right anterior oblique projection to adequately visualize both the interatrial septum and the intended point of puncture, the use of a pigtail catheter positioned in the ascending aorta to define the relation of the puncture site to the aorta in this projection and the utilization of a flexible preshaped guide wire to catheterize the left ventricle are the major factors contributing toward this improved success rate and low incidence of complications.


American Heart Journal | 1984

Comparison of the influence of acute transmural and nontransmural myocardial infarction on ventricular function

Pascal Nicod; James R. Corbett; C.Fagg Sanford; Jhulan Mukharji; Gregory J. Dehmer; Charles H. Croft; Robert E. Rude; Samuel E. Lewis; James T. Willerson

In order to assess the relative impact on left and right ventricular function of nontransmural and transmural acute myocardial infarction (AMI), we performed radionuclide ventriculography in 86 patients (54 men and 32 women) within 16 hours after a first infarct. Nontransmural infarction was present in 19 patients (11 anterior and 8 inferior). Transmural infarction was found in 67 patients (30 anterior and 37 inferior). Left ventricular ejection fractions were higher (0.57 +/- .014 vs 0.46 +/- 0.14, p less than 0.005) and left ventricular end-systolic volume lower (29 +/- 11 vs 42 +/- 20 ml/m2, p = 0.013) in patients with nontransmural infarction compared to those with transmural infarction. Right ventricular ejection fraction also may have been different in the two groups (0.63 +/- 0.15 vs 0.55 +/- 0.13, p = 0.057). In patients with inferior infarction, left and right ventricular ejection fractions were similar in patients with nontransmural and transmural infarction (0.60 +/- 0.09 vs 0.55 +/- 0.10, p = 0.119 and 0.58 +/- 0.14 vs 0.51 +/- 12, p = 0.226). On the other hand, patients with anterior transmural infarction had lower left ventricular ejection fractions (0.36 +/- 0.12 vs 0.54 +/- 0.17, p = 0.003) but similar right ventricular ejection fractions (0.60 +/- 0.13 vs 0.66 +/- 0.14, p = 0.14) compared to those with nontransmural anterior infarction. In 29 additional patients with a history of previous infarction, no differences in any of the parameters studied were found between those with transmural and those with nontransmural infarcts.(ABSTRACT TRUNCATED AT 250 WORDS)


American Journal of Cardiology | 1984

Comparison of left ventricular function and infarct size in patients with and without persistently positive technetium-99m pyrophosphate myocardial scintigrams after myocardial infarction: Analysis of 357 patients☆

Charles H. Croft; Robert E. Rude; Samuel E. Lewis; Robert W. Parkey; W. Kenneth Poole; Corette B. Parker; Nl Fox; Robert Roberts; H. William Strauss; Lewis J. Thomas; Daniel S. Raabe; Burton E. Sobel; Herman K. Gold; Peter H. Stone; Eugene Braunwald; James T. Willerson

One hundred nine patients with persistently positive technetium-99m pyrophosphate (Tc-99m-PPi) myocardial scintigrams 6 months after acute myocardial infarction (MI) (Group A) and 185 patients without such persistently positive scintigrams (Group B) were compared with regard to enzymatically determined infarct size, early and late measurements of left ventricular (LV) function determined by radionuclide ventriculography, and preceding clinical course during the 6 months after MI. The CK-MB-determined infarct size index in Group A (17.4 +/- 10.6 g-Eq/m2) did not differ significantly from that in Group B (16.0 +/- 14.6 g-Eq/m2). Similarly, myocardial infarct areas in the 2 groups, determined by planimetry of acute Tc-99m-PPi scintigrams in those patients with well-localized 3+ or 4+ anterior pyrophosphate uptake, were not significantly different (35.7 +/- 13.4 vs 34.4 +/- 13.1 cm2, respectively). However, patients in Group A had significantly lower LV ejection fractions than those in Group B, both within 18 hours of the onset of MI (0.42 +/- 0.14 vs 0.49 +/- 0.14, p less than 0.01) and at 3 months after MI, both at rest (0.42 +/- 0.14 vs 0.51 +/- 0.14, p less than 0.01) and at maximal symptom-limited supine bicycle exercise (0.44 +/- 0.17 vs 0.51 +/- 0.17, p less than 0.01). Peak exercise levels achieved in the 2 groups were not significantly different. Furthermore, patients in Group A demonstrated a greater incidence of congestive heart failure during the initial hospital admission (41 vs 24%; p less than 0.01) and a greater requirement for digoxin (p less than 0.05) and furosemide (p less than 0.01) after discharge.(ABSTRACT TRUNCATED AT 250 WORDS)


American Journal of Cardiology | 1986

Late thrombotic obstruction of aortic porcine bioprostheses

Charles H. Croft; L. Maximilian Buja; Manuel Z. Floresca; Pascal Nicod; Aaron S. Estrera


American Journal of Cardiology | 1982

Detection of right ventricular infarction by right precordial electrocardiograms

Charles H. Croft; Pascal Nicod; Samuel E. Lewis; James T. Willerson; Robert E. Rude


American Journal of Cardiology | 1984

Internal mammary arteriovenous fistula

Leo Finci; Raymond Maendly; Axel Essinger; Charles H. Croft; Pierre Magnenat; Pascal Nicod

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Robert E. Rude

University of Texas Health Science Center at San Antonio

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Samuel E. Lewis

Parkland Memorial Hospital

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Jhulan Mukharji

Parkland Memorial Hospital

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Pascal Nicod

Parkland Memorial Hospital

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James R. Corbett

Parkland Memorial Hospital

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Lewis J. Thomas

Parkland Memorial Hospital

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Robert Roberts

University of Texas Health Science Center at Houston

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H. William Strauss

Memorial Sloan Kettering Cancer Center

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