Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-seven patients (15 men, 12 women; mean age 48.9 years) suffering from ventricular tachycardia (VT) (n = 30) were studied by radionuclide angiocardiography with Fourier phase analysis, both in sinus rhythm and during tachycardia. VT was spontaneous, electrically inducible, sustained, haemodynamically stable and monomorphous, with a mean rate of 174 beats/min (range: 115-260 beats). Heart diseases responsible for VT were: non-obstructive cardiomyopathy (n = 7), hypertrophic cardiomyopathy (n = 1), ischaemic heart disease (n = 5), probable right ventricular arrhythmogenic dysplasia (n = 4), congenital left ventricular aneurysm (n = 2), sequela of myocarditis (n = 2) and aortic valve regurgitation (n = 1); no heart disease was detectable in 5 patients. On surface electrocardiogram there was good concordance between the initial radionuclide site of VT activation and the configuration and electrical axis of QRS. At Fourier phase analysis all 17 VT of the right lag type originated in the left ventricle, arising from the apical septum (n = 7) or lateral segment (n = 2) in case of left axis, from the basal segment (n = 6) or the lateral segment (n = 1) in case of vertical or right axis, and from the middle left septum (n = 1) in case of normal axis. Nine VT of the left lag type originated in the right ventricle, arising from the basal septum or the latero-basal region in case of vertical or right axis (n = 6), from the apical septum or the inferior-apical region in case of left axis (n = 2) and from the middle septum in case of normal axis (n = 1). Four of our patients (3 with coronary disease and 1 with congenital left ventricular aneurysm) had VT of the left lag type and an initial radionuclide site of activation in the middle part of the left septum in case of left axis (n = 2) and in the basal part of that septum in case of right axis (n = 2). Seven patients were operated upon for recurrent VT: 4 had intra-operative mapping which in every case confirmed the results of radionuclide angiocardiography, a method which in the other 3 patients was the only surgeon's guide. Correlations between the site of origin of VT at radionuclide mapping and kinetic abnormalities visualized at radiological angiography and gamma-ray angiocardiography were common in our study. In one of our patients the same lesion gave birth to 2 VT of different morphologies.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Isotope angiocardiographic study of 30 cases of ventricular tachycardia with Fourier phase analysis]. 313 7

Development of mitral regurgitation (MR) during acute myocardial ischemia is a well known occurrence. To assess the feasibility and clinical utility of detecting MR during exercise testing, color Doppler examinations were performed in 22 patients with angiographically proved coronary artery disease (CAD) and in 17 normal subjects before, during and after graded supine bicycle exercise. Not only was MR visualized using color Doppler during dynamic testing, but it was also slightly more sensitive (59% vs 54%) and specific (100% vs 88%) than the electrocardiographic response in identifying patients with CAD. When the appearance of MR or diagnostic electrocardiographic changes or both were used to identify patients with CAD, the sensitivity of exercise tolerance testing increased to 82%, although the specificity was 88%. In addition, exercise-induced MR was observed to be as sensitive and specific as exercise-induced wall motion abnormalities. Combining exercise-induced MR with wall motion abnormalities also increased the sensitivity to 82%, with the specificity remaining at 100%. With use of exercise-induced MR, wall motion abnormalities or electrocardiographic changes, the sensitivity and specificity of the exercise test in diagnosing CAD was 91% and 88%, respectively. The degree of MR as estimated by maximal area of regurgitation signals, as well as by its ratio to left atrial area, did not correlate with extent of CAD. However, the presence of exercise-induced MR suggested an increased likelihood of 3-vessel CAD because it was found in 9 of 11 patients with 3-vessel CAD, compared with 2 of 5 patients with 2-vessel and 2 of 6 patients with 1-vessel CAD.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Color Doppler assessment of mitral regurgitation induced by supine exercise in patients with coronary artery disease. 329 23

Pathologic studies of floppy or myxomatous mitral valves have focused primarily on changes in the valve cusps, with little attention given to the chordae tendineae. In a systematic study of the histopathology of floppy mitral valve chordae tendineae, 128 nonruptured chordae from 8 severely regurgitant floppy mitral valves were compared to 152 chordae from 10 normal control mitral valves and to 152 chordae from 8 control mitral valves with severe regurgitation due to ischemic heart disease. Collagen alterations were observed in 2% of normal mitral valve chordae and 3% of control regurgitant mitral valve chordae compared to 38% of floppy mitral valve chordae. Moderate or severe acid mucopolysaccharide accumulation was observed in 2% of normal mitral valve chordae and 3% of control regurgitant mitral valve chordae compared to 39% of floppy mitral valve chordae. Nonuniform histopathologic alterations, rare in normal and control regurgitant mitral valve chordae tendineae, were frequent in floppy mitral valve chordae tendineae (p less than 0.001). Histopathologic alterations provide the basis for abnormal physical properties previously demonstrated in floppy mitral valve chordae tendineae and may predispose to chordal elongation and rupture.
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PMID:Floppy mitral valve chordae tendineae: histopathologic alterations. 337 74

Vasodilator therapy of heart failure has through the last 5-10 years become a well established treatment. Traditionally these drugs have been classified after their primary site of action on the vascular beds. Thus drugs primarily acting on the arteriolar bed are called afterload-reducing agents and are exemplified by hydralazine. Drugs primarily acting on the venous bed have been called preload-reducing reducing agents and the typical example is nitroglycerin. Other drugs, like prazosin, act on both the arteriolar and venous vascular beds. The classification is, however, not as sharp as originally believed since preload- and afterload-reducing activities mix with each other. Treatment with vasodilators for chronic heart failure has mainly been advocated in patients with valvular regurgitation, ischemic heart disease and various types of dilated cardiomyopathies. It seems appropriate today to put some questions concerning vasodilator therapy for heart failure. Among such questions are: When in the natural history of congestive heart failure should vasodilator therapy be commenced? How effective is long-term administration of vasodilating drugs? May vasodilator therapy decrease mortality in congestive heart failure? What about the efficacy of new vasodilating drugs compared to more traditional ones? In the review of vasodilating drugs besides ACE inhibitors, these questions will be addressed.
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PMID:Aspects on "traditional" vasodilators in the treatment of chronic heart failure. 352 22

Forty-three patients with dilated cardiomyopathy (DCMP) and 12 patients with ischaemic heart disease (HD) in different stages of heart failure were examined using ultrasound sector scanning and pulsed Doppler echocardiography. The degree of mitral regurgitation was determined semi-quantitatively, according to the distance at which the turbulent blood stream penetrates into the left atrial cavity. The dimensions of the left atrium and auscultatory manifestations are not always a reliable indicator of the degree of regurgitation. The severity of mitral regurgitation depends on the dilatation and reduced contractility of the left ventricle as well as on the dilatation of the mitral annulus. Segmental contractility of the left ventricle was assessed using computer analysis of two-dimensional EchoCG. A characteristic feature of DCMP is not only a diffuse decrease in left ventricular contractility but also its segmental disturbances. These disturbances are in DCMP the same as in IHD, but in patients with DCMP there is no simultaneous occurrence of normokinetic and dyskinetic segments.
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PMID:The use of two-dimensional and Doppler echocardiography in assessing mitral regurgitation and segmental contractility disturbances in patients with dilated cardiomyopathy and ischaemic heart disease. 382 85

The clinical diagnosis of tricuspid regurgitation (TR) is often difficult. Two-dimensional pulsed Doppler echocardiography offers a sensitive and specific method for detecting and semi-quantitating tricuspid regurgitation. The clinical, radiographic, radionuclide, echocardiographic, and when available, the right cardiac catheterization findings were evaluated in 36 patients with a diagnosis of tricuspid regurgitation by pulsed Doppler. Ten healthy subjects served as controls. The underlying cardiac cause was rheumatic heart disease in 7 (20%), ischemic heart disease in 12 (33%), dilated cardiomyopathy in 5 (14%), hypertensive heart disease in 2 (5%), aortic valve stenosis and/or regurgitation in 3 (8%), mitral valve prolapse with mitral regurgitation in 1 (3%), and congenital heart disease in 6 (17%). Seven patients (19%) had a temporary or permanent transvenous right ventricular pacing wire. A systolic murmur was heard in 29 patients (81%) with 16 (46%) having an elevated jugular venous pressure. Tricuspid regurgitation was clinically suspected in only 2 patients (6%). Isolated tricuspid regurgitation was uncommon, seen in 6 patients (17%), and usually secondary to congenital heart disease, ischemic heart disease, with the use of a transvenous pacing wire and following mitral valve replacement. Right cardiac catheterization was performed in 10 patients, of which 7 demonstrated elevated right atrial and pulmonary artery pressure. Pulsed Doppler echocardiography offers a practical and accurate method of detecting and evaluating the severity of tricuspid regurgitation. Tricuspid regurgitation is generally a functional disorder, and frequently occurs in association with left sided valvular heart disease, cardiomyopathy or congenital heart disease.
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PMID:The clinical spectrum of tricuspid regurgitation detected by pulsed Doppler echocardiography. 390 35

The main blood flow velocity patterns in the LVOT and RVOT were recorded by pulsed Doppler echocardiography in 28 normal healthy cases, in two athletes, and in 85 patients with atrial septal defects, pulmonary regurgitation, tetralogy of Fallot, aortic regurgitation, mitral stenosis, aortic stenosis, mitral regurgitation, hypertrophic cardiomyopathy, ischemic heart disease, and pulmonary hypertension. Blood flow velocities were displayed using a graphic system to form a real time sonogram, using Fast Fourier Transformation. In the normal group, the blood flow velocity was 1.69 KHz in LVOT, and 1.71 KHz in RVOT. In AR and T/F but not MS, there was high blood flow velocity in the LVOT, and the peak of blood flow velocity was shifted to mid-to late systole. In ASD and VSD with a L-R shunt, high blood flow velocity occurred in the RVOT, and the peak velocity shifted to early systole. Pulmonary hypertension occasionally produced a W- or V-shaped curve. In normal subjects, a small "a" wave could be detected in the LVOT recording. The "a" wave began at point B on the AML tracer of the M-mode echocardiography, reached maximum velocity at point C, and returned to zero (baseline) at point C'. The "a" wave was coincident with the R wave of the ECG, and with the Ia of the phonocardiogram (PCG). The normal velocity of the "a" wave was 602 Hz, and the a/H ratio was 0.36. In cases of HCM and IHD, the "a" wave velocity and the a/H ratio correlated with the end diastolic pressure and the peak dP/dT. These data suggest that the Doppler blood flow patterns in the LVOT and RVOT can indicate volume overload in the right and left ventricles, and that the "a" wave velocity and a/H ratio can provide new information concerning cardiac performance.
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PMID:Main systolic blood flow patterns in the left and right ventricular outflow tracts determined by Doppler echocardiography. 404 Jul 20

Protecting the patient's airway is of paramount importance in the induction of general anesthesia. For the patient at risk of regurgitation of stomach contents, the rapid-sequence (crash) induction provides protection, but at the expense of increased stress response to laryngoscopy and intubation. This stress response is especially dangerous for the patient at risk for myocardial ischemia. The purpose of this study was to examine the efficacy of using low-dose fentanyl (5 micrograms/kg) to reduce cardiovascular and neuroendocrine stress responses to rapid-sequence induction. Thirty patients were randomly assigned to a rapid-sequence induction protocol either with or without fentanyl preloading. Fentanyl-preloaded patients (fentanyl group) received 2 mg/kg of thiopental whereas patients who were not preloaded with fentanyl (control group) received 4 mg/kg of thiopental. Data collected as indices of the stress response included heart rate, systolic, diastolic, and mean blood pressures, and plasma concentrations of catecholamines (epinephrine, norepinephrine, dopamine) and beta-endorphin. Electrocardiograms (modified V5 lead) were monitored for dysrhythmias and ST segment depression. Control patients had higher systolic, diastolic, and mean blood pressures after intubation than did patients given fentanyl (P less than 0.05). Although the incidence of dysrhythmias was decreased by fentanyl (20% vs 42%), this difference was not statistically significant. Plasma concentrations of beta-endorphin and norepinephrine increased significantly in control patients but not in patients given fentanyl (P less than 0.05). Low-dose fentanyl (5 micrograms/kg) reduces some aspects of the stress response to rapid-sequence induction of anesthesia.
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PMID:Fentanyl preloading for rapid-sequence induction of anesthesia. 631 5

Eighteen patients with clinical signs suggesting severe mitral regurgitation secondary to ischaemic heart disease were assessed by echocardiography. Non-ischaemic diseases needing specific therapy were revealed in six patients. In the other 12 patients echocardiography demonstrated myocardial lesions explaining the mitral regurgitation. Apart from the distinction between non-ischaemic conditions and lesions induced by ischaemia, echocardiography seems to be helpful in the demonstration of severe yet operable mitral valve regurgitation due to a small ischaemic lesion. Such cases are opposed to functional mitral regurgitation caused by extensive myocardial injury as demonstrated by two-dimensional echocardiography and reflected by a minimum mitral valve/septum separation of more than 2 1/2 cm on the M-mode echocardiogram. These conditions make symptomatic improvement by mitral valve surgery unlikely and carry an extremely high operative mortality. A more precise definition by heart catheterization is required when serious clinical heart failure is not explained by the echocardiographic finding of severe global myocardial impairment.
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PMID:Clinically suspected severe ischaemia-induced mitral regurgitation. Spectrum of lesions and features of high surgical risk by echocardiography. 649 83

Pulsed doppler echocardiography (PDE) was used to evaluate mitral regurgitation (MR) non-invasively and quantitatively in 156 patients including 51 of rheumatic valvular disease, 57 of mitral valve prolapse (MVP) or chordal rupture of the mitral valve (RCT), and 48 of ischemic heart disease (IHD) or dilated cardiomyopathy (DCM). The severity of MR was estimated three-dimensionally by a MR scoring system as follows: As an index of direction and extent of regurgitation, nine sampling sites were selected in the left atrium at the level of the mitral annulus. These include the anterior, mid, and posterior parts of each portion of the postero-medial, middle, and antero-lateral sides. The depth of regurgitation was graded by three degrees in the long-axis projection of the left ventricle; grade 1; MR signals localized within the level of the mitral annulus, grade 2; MR detected beyond the mitral annulus but not reaching the aortic valve level; and grade 3; MR detected beyond the aortic valve level in the left atrium. The MR score was comprised of the products of numbers of points at which MR signals were detected and the grades of the maximum depth. The MR scores correlated well with the severity of MR as determined by the left ventriculogram (LVG); the MR score was 4.0 +/- 1.6 (mean +/- S.D.) points in grade 1; 9.6 +/- 2.6 points in grade 2; 18.0 +/- 3.2 points in grade 3; and 23.0 +/- 1.7 points in grade 4 by LVG. Doppler mapping of the left atrium at the level of the mitral annulus suggested that the directions of MR varied with each disease and valvular lesion. Thus, these observations were helpful in the investigation of MR by PDE. We concluded that the above-mentioned MR scoring system proves a very useful method for quantitatively evaluating MR non-invasively.
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PMID:[Three-dimensional evaluation of mitral regurgitation by pulsed Doppler echocardiography: analysis of the amount and direction of regurgitant flow]. 654 71


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