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Dive into the research topics where Gerasim Tikoff is active.

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Featured researches published by Gerasim Tikoff.


The American Journal of Medicine | 1965

Heart failure in atrial septal defect

Gerasim Tikoff; Alexander M. Schmidt; Hiroshi Kuida; Hans H. Hecht

Abstract The hemodynamic data procured in thirtytwo adults with large atrial septal defects are reviewed and compared with those from six cases in children in whom atrial septal defect was complicated by pulmonary stenosis. Elevated right atrial pressure was a common finding in the adults. In the absence of mitral stenosis or constrictive pericarditis, elevation of right atrial pressure in large atrial septal defects may be considered a sign of left ventricular failure. Right ventricular failure in atrial septal defect is characterized by a decrease in the left-to-right shunt, appearance of a right-to-left shunt and a decrease in right ventricular forward output. All this occurs at normal pressures in the common atrium. Biventricular failure, occurring together or in sequence, is a common complication of atrial septal defect in the adult.


The American Journal of Medicine | 1969

Hemodynamic effects of exercise in patients with aortic stenosis

Fred L. Anderson; Theofilos J. Tsagaris; Gerasim Tikoff; Joseph L. Thorne; Alexander M. Schmidt; Hiroshi Kuida

Abstract Hemodynamic data obtained by right and left heart catheterization at rest and during exercise in thirty-two patients with aortic stenosis were reviewed. Eighteen patients had either minimal or no aortic regurgitation (group I) and fourteen patients had moderate to moderately severe aortic regurgitation (group II). The mean systolic pressure gradient (ΔP) across the aortic valve decreased or remained unchanged during exercise in eleven of eighteen patients in group I and in nine of fourteen patients in group II. Net forward aortic valve systolic flow (AVSF) increased during exercise in fourteen of eighteen patients in group I and in thirteen of fourteen patients in group II. Thus, in some patients the change in ΔP during exercise appears to be at variance with the predictability implied by the Gorlin equation which states that ΔP should be directly related to (AVSF) 2 . It is unlikely that this discrepancy can be explained on the basis of a systematic measuring error involving one or more of the various factors in the equation. This suggests that the aortic valve may not behave as a fixed orifice under all hemodynamic conditions, and that orifice hydraulics might be different depending on the mechanics of contraction. Average cardiac index (CI) was 2.5 L. per minute per M 2 . at rest and 3.8 L. per minute per M 2 . during exercise for patients in group 1, and 2.2 L. per minute per M 2 . at rest and 3.9 L. per minute per M 2 . during exercise for patients in group 2. Arterial and left ventricular systolic and diastolic pressures increased, and systemic resistance decreased during exercise. Thus, resting cardiac output is maintained and it increases during exercise at the expense of marked elevation in both systolic and diastolic pressures in the left ventricle. An analysis of the relationship between stroke work index (SWI) and left ventricular end diastolic pressure (LV edp ) in patients from group I revealed, in general, two types of responses to exercise. Six patients had an increase in SWI averaging 39 per cent associated with a 67 per cent increase in LV edp . In sharp contrast, ten other patients demonstrated an increase in SWI averaging only 1.3 per cent whereas LV edp increased by an average of 129 per cent. It is apparent therefore that the response to exercise makes it possible to separate patients with remaining myocardial reserve from those without. Thus, exercise data in patients with aortic stenosis provide objective, quantitative information useful in making a decision when and if to perform corrective surgery.


The American Journal of Medicine | 1967

Clinical and physiologic sequelae of large ventricular septal defects.

Gerasim Tikoff; Alexander M. Schmidt; Joseph L. Thorne; Hiroshi Kuida

Abstract The clinical and hemodynamic data in twenty-nine patients with large ventricular septal defects are analyzed. Evidence of heart failure is uncommon in those with pulmonary vascular disease and/or pulmonic stenosis alone, in contrast to those in whom certain other additional congenital lesions are present. These data are analyzed in terms of a physiologically single ventricle which exists when a large ventricular septal defect is present. Obligatory beat to beat synchronicity of the right ventricular and systemic arterial systolic pressure is discussed and its use in the diagnosis of the physiologically single ventricle in man outlined. Evidence is presented that in the face of a physiologically single ventricle, ventricular failure is most likely to occur when a volume or flow load is present in addition to right ventricular hypertension. The evolution and hemodynamic recognition of ventricular failure in the face of a physiologically single ventricle is discussed.


The American Journal of Medicine | 1969

Patent ductus arteriosus complicated by heart failure: Classification based on clinical and serial hemodynamic studies

Gerasim Tikoff; H.Mario Echegaray; Alexander M. Schmidt; Hiroshi Kuida

A heterogeneous group of four patients with patent ductus arteriosus and heart failure is described and the data from their serial hemodynamic studies are discussed. The evolution and etiology of heart failure in patients with patent ductus arteriosus is variable and is discussed in terms of a classification based on both the size of the defect and the degree of coexisting pulmonary vascular resistance. The hemodynamic evolution of heart failure is shown to be a relatively slow process. Coexisting features which may modify the evolution of failure are semilunar valvular insufficiency, a coexisting ventricular septal defect and possibly the volume of packed red cells.


American Journal of Cardiology | 1967

Isoproterenol-induced right ventricular infundibular obstruction: Study in adult with a large ventricular septal defect☆

Gerasim Tikoff; Alexander M. Schmidt; Theofilos J. Tsagaris

Abstract Clinical and hemodynamic data concerning a 31 year old man with a large ventricular septal defect, pulmonary hypertension and unexplained syncope are presented and discussed. Significant right ventricular outflow obstruction was not present during a control period or following the injection of tolazoline hydrochloride; however, right ventricular infundibular stenosis was elicited during the administration of isoproterenol. The significance of these findings is discussed.


JAMA Internal Medicine | 1976

Noninvasive Diagnosis of Deep Venous Thrombosis

Kent L. Richards; John D. Armstrong; Gerasim Tikoff; Edward J. Hershgold; Jeffrey L. Booth; Jack B. Rampton


The American review of respiratory disease | 1981

Venous thromboembolism in decompensated chronic obstructive pulmonary disease. A prospective study.

Stephen M. Prescott; Kent L. Richards; Gerasim Tikoff; John D. Armstrong; John W. Shigeoka


JAMA Internal Medicine | 1968

Atrial Fibrillation in Atrial Septal Defect

Gerasim Tikoff; Alexander M. Schmidt; Hans H. Hecht


Archive | 1965

Heart Failure in Atria1 Septal Defect

Gerasim Tikoff; Alexander M. Schmidt; Hiroshi Kuida; Hans H. Hecht


The American review of respiratory disease | 2015

Familial Primary Pulmonary Hypertension1, 2

Theofilos J. Tsagaris; Gerasim Tikoff

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