bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hemodynamic, anti‐ischemic, and neurohumoral effects of slow‐release isosorbide‐5‐mononitrate in patients with coronary artery disease after short‐ and long‐term therapy
Authors: Mitrovic V. , Gessner C. , Hain P. , Müller K. D. , Schlepper M. 
Published: February 2009

AbstractIn 20 patients with established coronary artery disease, stable angina pectoris and reproducible ST‐segment depression, the pharmacokinetics and pharmacodynamic effects of 60 mg slow‐release isosorbide‐5‐mononitrate (IS‐5‐MN) (10 patients) after a 7‐day therapy were compared with those of a placebo group (10 patients) using a randomized double‐blind, placebo‐controlled study design. Ten patients could be controlled after long‐term therapy over a mean of 399 ± 111 days. There was no significant change under IS‐5‐MN of either blood pressure, heart rate, rate–pressure product, or myocardial oxygen consumption. Treatment over one week significantly reduced ST‐segment depression 4 and 8 h after drug intake (38–48% of the placebo value, p<0.01). Maximum reduction in ST‐segment depression was found 4 and 8 h after IS‐5‐MN intake both after one‐week and long‐term therapy at the time of peak plasma drug concentration (341 ± 95 and 405 ± 125 ng/ml, respectively). At a residual plasma concentration below 100 ng/ml, ST depression was not significantly improved 24 h after drug intake compared with placebo. Technetium‐99m ventriculography showed an insignificant increase in ejection fraction and a slight reduction of ventricular volumes after both short‐ and long‐term therapy with IS‐5‐MN (p>0.05). The drug's plasma levels were higher under chronic than under short‐term therapy which may be due to enzyme saturation. Maximum IS‐5‐MN plasma concentrations at a mean of 445 ± 116 ng/ml were reached after 5.8 ± 2.9 h. Beta‐phase half‐life of elimination was 9 ± 3 h. IS‐5‐MN administered as a single 60 mg dose of a slow‐release preparation/day proved to have a favorable pharmacokinetic profile as well as an efficient anti‐ischemic activity after both short‐ and long‐term therapy. Problems of tolerance or activation of hormonal counter‐regulation due to vasodilation were not observed.
Acute and chronic effects of nitrendipine in patients with precapillary pulmonary hypertension due to pulmonary fibrosis
Authors: Burger W. , Jandl M. , Kober G. , Schultze‐Werninghaus G. , Gellert J. 
Published: February 2009

AbstractEleven patients with histologically confirmed fibrosis of the lung were investigated for the effects of the dihydropyridine calcium antagonist nitrendipine on pulmonary hemodynamics. After 5 mg of acute sublingual nitrendipine, mean pulmonary artery pressure was significantly lowered (p≤0.05) from 32 ± 3 to 29 ± 3 mmHg at rest, and significantly lowered (p≤0.05) during exercise from 55 ± 4 to 49 ± 4 mmHg. Short‐term oxygen application at rest significantly reduced this parameter to 28 ± 3 mmHg(p≤0.01). Nitrendipine lowered total pulmonary vascular resistance during both rest (from 412 ± 50 to 351 ± 49 dyn•S•cm‐5; p≤0.05) and exercise (from 433 ± 61 to 383 ± 54 dyn•s•cm‐5; p≤0.05), although it did not affect pulmonary arteriolar resistance. Also, oxygen treatment at rest influenced only total pulmonary vascular resistance (reduction from 412 ± 50 to 373 ± 48 dyn•s•cm‐5; p≤0.01), but not pulmonary arteriolar resistance. Pressure‐flow curves, which were derived from cardiac output at rest and during exercise and from the corresponding gradient between mean pulmonary artery pressure and pulmonary capillary wedge pressure, remained unchanged by acute medication. Since a change in arterial oxygen partial pressure was not noticed after nitrendipine, arteriovenous shunting or a worsening of ventilation perfusion relationships can be excluded. Long‐term (3 weeks) treatment (double‐blind parallel design) with 10 mg of nitrendipine (4 patients) once daily showed no advantage in comparison to placebo (6 patients). From these observations we conclude that the reduction of lower circulatory pressures after nitrendipine is not caused by pulmonary arteriolar vasodilation, but rather by indirect effects due to the reduction of total peripheral resistance and left ventricular filling pressure.
Negative u wave during percutaneous transluminal coronary angioplasty
Authors: Yano Hayato , Hiasa Yoshikazu , Aihara Tsukasa , Nakaya Yutaka , Mori Hiroyoshi 
Published: February 2009

AbstractTo clarify the clinical significance of the negative U wave during acute myocardial ischemia, the appearance of the U wave and ST‐segment elevation on electrocardiography during percutaneous transluminal coronary angioplasty (PTCA) of the left anterior descending artery (LAD group: 11 patients) or right coronary artery (RCA group: 18 patients) was studied. During PTCA, U‐wave inversion (newly developed negative U wave, and increased negativity of the pre‐existing negative U wave) was observed in 37 (90%) of 41 patients in the LAD group and in 16 (89%) of 18 patients in the RCA group. The incidence of ST‐segment elevation was similar to that of U‐wave inversion; however, U‐wave inversion appeared before detectable ST‐segment elevation in 20 patients (49%) in the LAD group and in 4 patients (22%) in the RCA group. Moreover, U‐wave inversion was observed frequently in a wider range of leads than ST‐segment elevation. These results suggest that the U wave is a more sensitive indicator of myocardial ischemia than ST‐segment elevation in some patients, and that a negative U wave may be produced by a different mechanism than that which produces ST‐segment deviation, although both are related to myocardial ischemia.
Antithrombotic therapy in the coronary vein graft patient
Authors: Israel Douglas H. , Fuster Valentin , Stein Bernardo , Adams Philip C. , Stein Bernardo , Chesebro James H. 
Published: February 2009

AbstractCoronary artery bypass grafting is an important therapeutic modality in the treatment of the patient with coronary artery disease; however, long‐term results are limited by the development of saphenous vein graft disease early and late after operation. The pathogenesis of early vein graft occlusion is primarily thrombotic, while that occurring later frequently involves thrombosis superimposed on intimal hyperplasia or vein graft atherosclerosis. We describe the role of various platelet inhibitors and anticoagulants in the prevention of saphenous vein graft occlusion following coronary artery bypass grafting.
Long‐term clinical course of patients with angina and angiographically normal coronary arteries
Authors: Voelker Wolfram , Euchner Ulrich , Dittmann Herbert , Karsch Karl R. 
Published: February 2009

Abstract: In 88 of 103 consecutive patients with angina and normal coronary arteries, follow‐up data could be achieved 6–11 years (9.2 ± 1.2 years) after diagnostic left heart catheterization. Three of these patients died during follow‐up (two noncardiac deaths and one death with no identifiable etiology). One patient suffered a documented myocardial infarction. In 40 patients (47%) chest pain diminished, while symptoms were unchanged in 20 (24%) or even worse in 25 (29%). Resolution or persistence of chest pain could not be predicted either by the character of pain (typical vs. atypical), the presence of hypertension, a left bundle‐branch block, a positive exercise electrocardiogram or pathological pulmonary artery pressures during exercise, documentation of myocardial bridges, local wall motion abnormalities, or a left ventricular end‐diastolic pressure $$ 13 mmHg. However, continuing chest pain was significantly more common in patients who revealed a ‘slow‐flow phenomenon’ at initial coronary arteriogram.Thus, in patients with angina and normal coronary arteries the long‐term course regarding frequency of morbid cardiac events is benign. However, more than half of the patients reported chest pain to be similar or even worse than at catheterization. Most clinical and invasive results at initial evaluation had no predictive value for the persistence of symptoms. The impact of ‘slow‐flow’ in coronary arteriography, which was a phenomenon almost exclusive to patients with constant or even worse chest pain at follow‐up, should be evaluated in larger patients populations.
Symptomatic bradycardia induced by the combination of oral diltiazem and beta blockers
Authors: Sagie Alex , Strasberg Boris , Kusnieck Jairo , Sclarovsky Samuel 
Published: February 2009

AbstractTen patients, who were admitted to the Intensive Coronary Care Unit during a one year period with symptomatic bradycardia while on combination therapy with oral diltiazem and beta‐blocker agents, are described. The important features of this adverse reaction to drug combination were that it appeared mainly in a relatively elderly age group and with presenting symptoms of lethargy, dizziness, syncope, chest pain, and (in one patient with poor left ventricular function) pulmonary edema. It was not dose dependent and occurred even in very low doses of each drug. Electrophysiologic abnormalities were localized to the sinus node in all 10 patients and the primary rhythm disorders were junctional escape rhythm, sinus bradycardia, and sinus pause. These rhythm abnormalities resolved within 24 h following withdrawal of the offending drugs. Temporary pacemaker insertion was necessary in four patients. The duration of drug combination used before the acute episode range from within hours to up to 2 years. In conclusion, although combination diltiazem/beta blocker therapy is very effective in ischemic syndrome, caution is advised when this combination is used especially in the elderly or in patients with left ventricular dysfunction or antecedent sinoatrial or atrioventricular conduction abnormality.
Conservative treatment of paroxysmal ventricular tachycardia during pregnancy
Authors: Chandra Nisha Chibber , Gates Elena A. , Thamer Mahmud 
Published: February 2009

AbstractParoxysmal ventricular tachycardia during pregnancy presents a therapeutic dilemma for the treating physician. The clinical course of two otherwise healthy pregnant patients with this arrhythmia in whom treatment was withheld is outlined. The indications and guidelines for treatment in relatively asymptomatic patients is discussed.
The S wave in acute anterior Q‐wave myocardial infarction: A study with serial multilead precordial maps and standard ECGs
Authors: Madias John E. 
Published: February 2009

AbstractTo investigate the relationship of S waves with R waves and/or Q waves in the ECGs of patients with acute myocardial infarction, 20 patients with anterior Q‐wave infarcts had serial 49‐lead precordial maps and simultaneously recorded standard ECGs on admission and at 13 predetermined time intervals, extending to their discharge from the hospital. The sums of S waves (ΣS) from ECG leads of both precordial maps and standard ECGs showing ST‐segment elevation on admission were correlated with the corresponding sums of R waves ($$R) and/or Q waves ($$Q). Correlation of $$S by the precordial maps and the $$S by the standard ECG was good (r=0.88). However, correlation of $$S with $$R and $$Q by both the precordial maps and standard ECG were poor (r values ranged between –0.02 and –0.32). Fair correlations were found between $$S + $$Q and the corresponding $$R by both ECG systems (r=–0.36, precordial map and r= –0.40, standard ECG). The present study demonstrates (1) that precordial (consequently partial) ECG mapping systems have no advantage over standard precordial ECG, and (2) that quantitative data from S waves correlate weakly with similar information from corresponding R waves or Q waves, but fairly with the latter two combined, as recorded by the two ECG systems employed.
Doppler assessment of right ventricular filling dynamics during volume loading in ischemic heart disease
Authors: Odake M. , Takeuchi M. , Fukuzaki H. 
Published: February 2009

AbstractTo assess the effects of volume loading on right ventricular (RV) filling dynamics, the RV inflow pattern was recorded using pulsed Doppler echocardiography (PDE) during dextran infusion in 7 normal subjects (Group I) and 24 patients with ischemic heart disease. The patients with ischemic heart disease were divided into three groups according to the left ventricular (LV) and RV ejection fractions (EF). Group II consisted of 11 patients whose LVEF and RVEF exceeded 50%. Group III consisted of 7 patients whose LVEF was lower than 50% and RVEF was higher than 50%. Group IV was comprised of 6 patients whose LVEF and RVEF were lower than 50%. Peak flow velocity of the RV rapid filling wave in early diastole [R(T)] and that of the atrial contraction wave [A(T)] were measured, and the ratio of A(T) to R(T) [A(T)/R(T)] in each cardiac cycle was calculated. In some of the subjects, simultaneous right‐sided cardiac catheterization was performed with a Swan‐Ganz thermodilution catheter. The LV and RV function during volume loading were calculated according to the following formulae: $DL Stroke volume index (SVI)/$DL pulmonary artery wedge pressure (PAWP) and $DLSVI/$DLright atrial pressure (RAP), respectively. After dextran infusion, R(T) increased significantly in Groups I, II, and III, but not in Group IV. The A(T) and A(T)/R(T) ratio remained unchanged in all groups. The percent change of the R(T) correlated well with $DLSVI/$DLRAP (r=0.56, p>0.01). These results suggest that in patients with RV dysfunction, volume loading does not result in an increase in SVI, and this abnormality seems to be related to unchanged R(T) after volume loading because of impairment in RV early diastolic filling. Thus, the assessment of the RV inflow pattern by PDE during dextran infusion was useful in demonstrating RV diastolic dysfunction in IHD.
Left Ventricular Outflow Tract Obstruction in Atrioventricular Septal Defects: A Pathologic and Morphometric Evaluation
Authors: Gallo P. , Hokayem N. J. , D'Offizi F. , D'Alessandro  , Francalanci P. , D'Amati G. , Waller Bruce , Formigari R. , Colloridi V. , Pizzuto F. 
Published: February 2009

AbstractSummary: Subaortic stenosis has been described with increasing frequency as an ominous feature of atrioventricular septal defect (AVSD), especially following surgical correction of the anomaly in non‐Down's syndrome patients. In order to study the surgical anatomy of the left ventricular outflow tract in this malformation, 48 hearts featuring AVSD were examined. Obstructive lesions were classified into unequivocal forms (class A, 13.5%) and potential ones (class B, 10.8%). In the remaining hearts (class C, 75.7%) no obstruction was noted. In class A, subaortic stenosis was due to exaggeration of the anticipated anomalous arrangement of atrioventricular valve tensor apparatus, to the persistence of a subaortic muscular infundibulum, and to a discrete fibrous diaphragm. A potential for subaortic stenosis is provided by the unwedged position of the aortic valve. The left ventricular outflow tract is transformed into a long, forward‐displaced fibromuscular channel. Morphometric analysis showed in AVSD (with both common annulus and separate orifices) a significantly (p>0.01) lower inflow/outflow tract ratio, and a significantly (p>0.01) lower right ventricular/left ventricular outflow length ratio than normal hearts. These results suggest that AVSD is characterized not only, as commonly stated, by inflow tract shortening, but by outflow tract lengthening as well. On these anatomical grounds, nearly all cases of AVSD could harbor the potential for subaortic stenosis; however, this becomes a real hazard (class B) only when associated with forward displacement of the left anterior papillary muscle, or direct insertion on the ventricular septum of the anterior bridging leaflet, and it may be converted to an actual obstruction by the effects of surgery. A short axis pathologic and echocardiographic plane is proposed to evaluate the potential subaortic stenosis and its possible transformation into an actual one.
Double Aortic Arch, Tetralogy of Fallot with Pulmonary Atresia and Atrioventricular Septal Defect
Authors: Gnanapragasam James P. , Keeton Barry R. , Fong Lance V. 
Published: February 2009

AbstractSummary: A double aortic arch is usually an isolated abnormality. We describe a case with a previously undescribed combination of tetralogy of Fallot with pulmonary atresia, complete atrioventricular septal defect, and left patent arterial duct in association with a double aortic arch. A complete diagnosis was made by echocardiography. Meticulous suprasternal echocardiography must be employed to avoid overlooking an unsuspected aortic arch abnormality.
Unknown Extra Cardiac Echo‐Free Space: Diagnosis of a Left Ventricular Pseudoaneurysm by Color Flow Echocardiography
Authors: Weston Mark W. , Mckinnon Elizabeth , Donald Tommie , Vijayanagar R. , Canedo Mario 
Published: February 2009

AbstractSummary: At times, visualization of a ventricular pseudoaneurysm by two‐dimensional echocardiography can be difficult. This case report describes the unique diagnostic potential of color flow echocardiography in the diagnosis of an unknown extra cardiac echo‐free space, a left ventricular pseudoaneurysm. Using color Doppler echocardiography flow can be seen communicating between the left ventricle and the pseudoaneurysm.
Prazosin's Effect in High Renin Hypertension Complicating Pheochromocytoma
Authors: Rechavia E. , Mager A. , Sagie A. , Strasberg B. , Sclarovsky S. 
Published: February 2009

AbstractSummary: During three consecutive days of prazosin treatment in a patient with pheochromocytoma, urinary catecholamine metabolite levels were correlated with plasma renin activity. Suppression of renin plasma activity resulted in sustained hemodynamic and clinical improvement, while no remarkable changes were observed in urinary catecholamine metabolite levels. This suggests that prazosin may interrupt the vicious cycle of worsening hypertension provoked by further activation of the renin‐angiotensin system mediated by excessive circulating catecholamines.
Vasodepressor Syncope from Neck Cancer with Associated C‐6 Dermatome Neuralgia
Authors: Osborn Larry A. , Frierson John , Herzon Fred 
Published: February 2009

AbstractAn unusual case of neck cancer with associated C‐6 dermatome neuralgia causing vasodepressor syncope episodes is discussed. Pacemaker therapy proved not to be required. When evaluating syncope with bradycardia, it is important to search for underlying causes and to ascertain whether or not pacemaker therapy is indicated.
Sublingual Administration of Captopril in Patients with Acute Myocardial Ischemia
Authors: Haude Michael , Erbel Raimund , Steffen Wolfgang , Tschollar Werner , Meyer Jürgen 
Published: February 2009

AbstractSummary: To investigate the anti‐ischemic capability of the angiotensin‐converting enzyme inhibitor captopril, 10 patients with acute myocardial ischemia (angina pectoris >1 h, ST‐segment depression ±0.1 mV, no rise in creatine phosphokinase) received 25 mg captopril sublingually after being treated with an intravenous infusion of nitroglycerin (3 mg/h) and heparin (1200 IU/h) for 1 hour. A control group of 10 patients received placebo instead of captopril. Results showed a decrease of the initial ST‐segment depression from 0.25±0.04 to 0.2±0.03 mV (p>0.01) with nitroglycerin for the captopril group and from 0.26±0.05 to 0.21±0.05 mV (p>0.01) for the control group. An additional decrease to 0.13±0.03 mV (p>0.001) was measured after sublingual captopril, while no significant change was found in the placebo group (0.19±0.04 mV). In both groups, 3 patients had no incidents of angina after 1‐h nitroglycerin infusion. An additional 6 patients resolved their complaints after captopril administration in contrast to only 1 after placebo. Two patients in the placebo group required increased doses of nitroglycerin because of impairment of anginal complaints. Hemodynamic measurements documented a significant drop of pulmonary vascular resistance after a 1‐h infusion of nitroglycerin (–12.9% and –13.1%, respectively, p>0.05), while all other parameters remained unchanged. After additional sublingual administration of captopril, a significant increase in cardiac index (+13.8%, p>0.05) was measured and decreases in diastolic pulmonary and blood pressures (–19.2%, p>0.05 and –14.6%, p>0.01), systemic and pulmonary vascular resistance (–17.7%, p>0.01 and –13.6%, p>0.05), and heart rate pressure product (–8.8%, p>0.05), while no significant changes were measured in the control group. No patient suffered acute myocardial infarction during the study period.
Static Versus Dynamic Exercise: Effects on Doppler Echocardiographic Indices of Left Ventricular Performance
Authors: Bamrah Virinderjit S. , Sagar Kiran B. , Sheldahl Lois M. , Wann L. Samuel 
Published: February 2009

AbstractSummary: In order to compare the effects of static exercise with those of dynamic exercise on the Doppler echocardiographic measurements of ascending aortic blood flow velocity and acceleration, Doppler echocardiography was performed with sustained handgrip exercise and with supine bicycle exercise in 12 normal subjects, 12 patients with coronary artery disease, and 7 patients with heart failure. In normal subjects: peak velocity decreased by 16±11% with handgrip from the resting value and increased by 49±19% with bicycle exercise (p>0.01); mean acceleration decreased by 6±30% with handgrip and increased by 162±83% with bicycle exercise (p>0.01). In patients with coronary artery disease: peak velocity declined by 9±14% with handgrip and increased by 19± 18% with bicycle exercise (p>0.01); mean acceleration increased by 13±27% with handgrip and by 41 ±33% with bicycle exercise (NS). In patients with congestive heart failure: peak velocity decreased by 19±13% with handgrip and increased by 5±17% with bicycle exercise (p>0.01); mean acceleration decreased by 12±23% with handgrip and by 4±37% with bicycle exercise. A marked increase in afterload stress induced by static exercise presumably offsets the moderately increased contractility and accounts for the decline of peak velocity and mean acceleration with static exercise both in normals and cardiac patients. In contrast, marked increase in contractile state along with little change in afterload with dynamic exercise results in markedly increased peak velocity and mean acceleration in normal subjects. In cardiac patients, however, the increase in peak velocity and mean acceleration with dynamic exercise are blunted. The changes in peak velocity and mean acceleration with handgrip are similar in normal subjects and cardiac patients. On the other hand, changes in these variables with dynamic exercise are markedly different in normal subjects and cardiac patients. Doppler echocardiographically measured peak velocity and mean acceleration respond differently to static and dynamic exercise. Measurement of these variables with dynamic exercise is more useful in evaluating left ventricular systolic function than static exercise.