John P. Fisher

Hartford Hospital, Hartford, Connecticut, United States

Are you John P. Fisher?

Claim your profile

Publications (5)50.58 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Autopsy studies have suggested that infarction of > 35% of the myocardium is associated with cardiogenic shock. However, the relation between the extent of myocardial dysfunction and hemodynamic status has not been defined in patients in vivo. This study investigated, in patients with short-term and chronic left ventricular dysfunction, the relation between hemodynamic status and the extent of regional dyssynergia measured by two-dimensional echocardiography with quantitative endocardial surface mapping. Sixty patients were classified into hemodynamic groups by pulmonary capillary wedge pressure and cardiac index. Two-dimensional echocardiograms were used to calculate left ventricular endocardial surface area index (ESAi), abnormal wall motion index (AWMi), percentage myocardial dysfunction (%MD), and number of wall motion abnormalities. All patients in class 4 (high pulmonary capillary wedge pressure and low cardiac index had > or = 60% MD. With univariate analysis, hemodynamic class correlated with ESAi, AWMi, %MD, the number of wall motion abnormalities, and two clinical variables (number of infarctions and use of diuretic agents). By stepwise linear regression, only AWMi and the number of infarctions were independently predictive of hemodynamic status.
    American Heart Journal 07/1995; 129(6):1114-21. DOI:10.1016/0002-8703(95)90391-7 · 4.56 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Objectives. This study was designed to assess the feasibility of calculating left ventricular volumes using intracardiac ultrasound.Background. Previous studies have validated transthoracic echocardiographic determinations of left ventricular volumes and have indicated the superiority of Simpson rule reconstruction algorithms. The feasibility of imaging the left ventricle with intracardiac ultrasound has also been demonstrated.Methods. The determination of left ventricular volumes with Simpson rule reconstruction of intracardiac ultrasound images was evaluated in two phases. In vitro validation was performed in 29 animal hearts preserved in either a nondistended or distended state. Latex cast volumes were the reference standard. In vivo studies used 14 pigs, and compared intracardiac ultrasound volumes and ejection fraction with single-plane contrast angiographic values. A 12.5-MHz device was used to record short-axis images at 0.5-cm intervals. These were used to reconstruct the ventricle as a stack of cylindric elements using all imaged levels as well as sections recorded every 1 and 2 cm and at a single midventricular level.Results. In the in vitro hearts, when all recorded sections were used, there was excellent agreement between intracardiac ultrasound and latex cast volumes (intracardiac ultrasound volume = 0.89 latex cast volume + 2.22, r = 0.95; intracardiac ultrasound volume = 0.97 latex cast volume + 0.91, r = 0.99) for nondistended and distended hearts, respectively. In vivo, there was again close correspondence between ultrasound and angiographic volumes (intracardiac ultrasound volume = 1.04 angiographic volume −3.6, r = 0.91). The relation between intracardiac ultrasound and angiographic ejection fraction was fair (intracardiac ultrasound ejection fraction = 1.00 angiographic ejection fraction + 6.85, r = 0.69). Excellent correlations for the volumes were maintained as the number of cross sections was reduced to those recorded every 1 and 2 cm (r = 0.87 to 0.99). With a single midventricular site more variable but generally good correlations were obtained (r = 0.77 to 0.99).Conclusions. The application of Simpson rule reconstruction to short-axis images of the left ventricle obtained with intracardiac ultrasound provides accurate determination of left ventricular volumes in animal hearts. This technique may prove useful in the analysis of left ventricular structure and function.
    Journal of the American College of Cardiology 08/1994; DOI:10.1016/0735-1097(94)90570-3 · 15.34 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Objectives. The purpose of this study was to evaluate the efficacy of radiofrequency-powered thermal balloon angioplasty in an in vivo porcine model.Background. Various modes of thermal energy used adjunctively during balloon angioplasty have demonstrated the potential to enhance the results of acute lumen dilation.Methods. In normal pigs, 75 peripheral arteries were dilated with a newly designed, radiofrequency-powered, thermal angioplasty balloon. All inflations were performed at 2-atm pressure for 85 s. Dilations were performed either with (hot) or without (cold) the application of heat. Lumen dimensions and vessel morphology were assessed with intravascular ultrasonography. At the end of each study, dilated arterial segments were harvested for histologic examination.Results. Single cold balloon inflations resulted in a 12.7% increase in arterial cross-sectional area whereas single hot inflations resulted in a 22.9% increase (p < 0.03). Similarly, when multiple cold inflations were compared with multiple hot inflations, two, three and four sequential hot inflations resulted in a significantly greater increase in cross-sectional area than an equivalent number of cold inflations (p < 0.03).Histologic examination demonstrated a temperaturedependent effect on the depth of medial necrosis and extent of arterial wall thinning (p < 0.001) as well as evidence for uniform alteration of elastic tissue fibers at temperatures of ≥60 °C (p < 0.03).Conclusions. Low pressure radiofrequency thermal balloon angioplasty results in a greater increase in cross-sectional area in porcine peripheral arteries than does nonheated conventional balloon angioplasty. The pathologic basis for this enhanced dilation may be a temperature-dependent effect on medial necrosis, thinning of the arterial wall or alteration of vascular elastic fibers, alone or in combination.
    Journal of the American College of Cardiology 05/1993; 21(6-21):1512-1521. DOI:10.1016/0735-1097(93)90332-U · 15.34 Impact Factor
  • Journal of the American College of Cardiology 02/1991; 17(2). DOI:10.1016/0735-1097(91)92220-G · 15.34 Impact Factor