Clinical cardiology
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Clinical cardiology · May 1995
Review Case ReportsTorsade de pointes caused by high-dose intravenous haloperidol in cardiac patients.
Intravenous haloperidol is the agent of choice for controlling severe agitated delirium in seriously ill cardiac patients in many institutions. Prior reports have proposed that high-dose intravenous haloperidol may be without untoward effects in these patients. Recently, however, a few reports of significant QTc prolongation and torsade de pointes as complications of high-dose intravenous haloperidol therapy have appeared. ⋯ Neither electrolyte imbalance, therapy with other cardiac drugs, bradycardia, ischemia, left ventricular dysfunction, nor other known cause of torsade was present in these patients. It is hypothesized that QTc prolongation and torsade likely are idiosyncratic, unpredictable reactions to high-dose haloperidol in select patients. Careful serial electrocardiographic monitoring and prompt discontinuation of the drug should suffice to prevent this relatively uncommon, life-threatening complication of high-dose intravenous haloperidol.
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Clinical cardiology · Apr 1995
Pathology of tricuspid valve stenosis and pure tricuspid regurgitation--Part III.
This three-part article examines the histologic and morphologic basis for stenotic and purely regurgitant tricuspid valves. In Part III, morphometric analysis of tricuspid valve annular circumference, leaflet area, and the product of annular circumference and leaflet area are shown to be useful in establishing etiology for the purely regurgitant tricuspid valves and in assessing the anatomic basis of pure tricuspid regurgitation in the presence of mitral stenosis.
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Clinical cardiology · Mar 1995
ReviewPathology of tricuspid valve stenosis and pure tricuspid regurgitation--Part II.
This three-part article examines the histologic and morphologic basis for stenotic and purely regurgitant tricuspid valves. In Part I, conditions producing tricuspid valve stenosis were reviewed. ⋯ In contrast to the relatively few causes of tricuspid stenosis, the causes of pure (no element of stenosis) tricuspid regurgitation are multiple. Some of the conditions producing pure regurgitation include floppy tricuspid valves, infective endocarditis, papillary muscle dysfunction, rheumatic disease, and Ebstein's anomaly.
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Clinical cardiology · Feb 1995
ReviewPathology of tricuspid valve stenosis and pure tricuspid regurgitation--Part I.
This three-part article examines the histologic and morphologic basis for stenotic and purely regurgitant tricuspid valves. In Part I, conditions producing tricuspid valve stenosis are reviewed. ⋯ In isolated tricuspid stenosis, the etiology is either carcinoid or congenital. Rare causes of tricuspid stenosis include active infective endocarditis, metabolic or enzymatic abnormalities (Fabry's, Whipple's disease), and giant blood cysts.
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Clinical cardiology · Dec 1994
Comparative StudyNoninvasive evaluation of contractile state by left ventricular dP/dtmax divided by end-diastolic volume using continuous-wave Doppler and M-mode echocardiography.
The maximum rate of left ventricular (LV) pressure rise (dP/dtmax) is commonly used in the assessment of directional change in LV contractility and, recently, estimated by analyzing continuous-wave Doppler ultrasound velocity curve of mitral regurgitation. As an alteration in ventricular preload is known to affect dP/dtmax, normalized dP/dtmax for preload might be more reliable to assess LV contractile state. To investigate the usefulness of a new index of LV contractile state determined by continuous-wave Doppler analysis of mitral regurgitation and M-mode echocardiogram-derived LV end-diastolic volume, we studied 18 patients with mild mitral regurgitation. ⋯ Corrected Doppler-derived dP/dtmax for LV end-diastolic volume using Teichholz's method significantly increased by inotropic stimulation with dobutamine (p < 0.01); however, it remained unchanged by augmentation of afterload with angiotensin II. Thus, the LV dP/dtmax can be accurately estimated in humans by analyzing the continuous-wave Doppler velocity curve of mitral regurgitation, and corrected Doppler-derived dP/dtmax for LV end-diastolic volume is relatively independent of loading alteration and sensitive to inotropic stimulation. We concluded that echocardiographic assessment by combined Doppler- and M-mode measurements provides a useful and sensitive index of LV contractile state noninvasively.