Search PubMed⌕ Search

Biomedical subjects

M J Kern

Publications and source records attributed to M J Kern.

At least 253 records · Page 14Linked to original sources
PubMed1991

Attenuation of myocardial ischemia during coronary occlusion by ultrashort-acting beta adrenergic blockade.

To assess the effect of the ultrashort-acting beta blocker esmolol on ischemia induced by acute coronary occlusion, we studied 16 patients undergoing coronary angioplasty. Doppler echocardiography and ECG monitoring were performed continuously before, during, and after balloon occlusion in the drug-free state and during esmolol infusion. Fourteen of the 16 patients had ST segment elevation during balloon inflation. However, maximal ST segment elevation (2.1 +/- 1.5 mm vs 1.7 +/- 1.3 mm, p less than 0.001) and duration of ST segment elevation (68 +/- 20 seconds vs 54 +/- 19 seconds, p less than 0.05) were both significantly reduced during esmolol infusion. Furthermore, the decrease in ejection fraction seen during drug-free balloon occlusions was significantly blunted during esmolol infusion. In the baseline state ejection fraction decreased from 55% to 38% (p less than 0.05) during coronary occlusion compared with a decrease from 52% to 49% (p = NS) during esmolol infusion. In addition, esmolol appeared to delay the onset of segmental wall motion abnormalities after coronary occlusion, occurring at a mean of 40 seconds after balloon inflation versus a mean of 31 seconds in the absence of beta blockade (p less than 0.05). Thus the use of ultrashort-acting beta blockade appears to diminish the extent and delay the onset of myocardial ischemia during acute coronary occlusion.

Adrenergic beta-Antagonists↗
PubMed1991

The effects of high (sodium meglumine diatrizoate, Renografin-76) and low osmolar (sodium meglumine ioxaglate, Hexabrix) radiographic contrast media on diastolic function during left ventriculography in patients.

Although a majority of studies indicate superior hemodynamic and clinical profiles of low osmolar compared with high osmolar contrast media, the effect of these agents on diastolic left ventricular function has not been examined. We prospectively examined hemodynamic, electrocardiographic, and echocardiographic indices of left ventricular function in patients undergoing contrast ventriculography with a high osmolar, ionic, monomeric contrast, diatrizoate (Renografin-76) compared with a low osmolar, ionic, dimeric contrast, ioxaglate (Hexabrix). Thirty patients were randomized to each group. There were no clinical differences between the two groups. The decrease in systemic pressures was significantly greater with diatrizoate after left ventriculography (-38.5 +/- 3.5 versus -18.2 +/- 2.3, p less than 0.001) and selective left coronary angiography (-29.5 +/- 2.4 versus -17.4 +/- 2.6, p less than 0.001). In addition, left ventricular end-diastolic pressure increased significantly more with diatrizoate (7.3 +/- 0.9 versus 2.7 +/- 0.8 mm Hg for ioxaglate, p less than 0.001). QT interval prolongation occurred in both patient groups. Diatrizoate decreased systemic vascular resistance, and increased cardiac output and left ventricular ejection fraction more than ioxaglate, while simultaneously increasing left ventricular end-diastolic volume and altering the peak atrial filling velocity. Negative dp/dt (p less than 0.05), but not Tau, computed by the logarithmic or derivative methods, was reduced by diatrizoate. These data indicate that significant alteration of diastolic filling patterns occurs with high osmolar compared with low osmolar contrast agents. Although the clinical significance of this observation is currently unknown, these data further support the reported hemodynamic superiority of the low osmolar, dimeric contrast agent ioxaglate during contrast angiography.

Contrast Media↗
PubMed1991

Intravenous adenosine: continuous infusion and low dose bolus administration for determination of coronary vasodilator reserve in patients with and without coronary artery disease.

To assess the use of adenosine as an alternative agent for determination of coronary vasodilator reserve, hemodynamics and coronary blood flow velocity were measured at rest and during peak hyperemic responses to continuous intravenous adenosine infusion (50, 100 and 150 micrograms/kg per min for 3 min) and intracoronary papaverine (10 mg) in 34 patients (17 without [group 1] and 17 with [group 2] significant left coronary artery disease), and in 17 patients (11 without and 6 with left coronary artery disease) after low dose (2.5 mg) intravenous bolus injection of adenosine. The maximal adenosine dose did not change mean arterial pressure (-10 +/- 14% and -6 +/- 12% for groups 1 and 2, respectively) but increased the heart rate (15 +/- 18% and 13 +/- 16, respectively). For continuous adenosine infusions, mean coronary flow velocity increased 64 +/- 104%, 122 +/- 94% and 198 +/- 59% and 15 +/- 51%, 110 +/- 95% and 109 +/- 86% in groups 1 and 2, respectively for each of the three doses. Mean coronary flow velocity increased significantly after 100 and 150 micrograms/kg of adenosine and 10 mg of intracoronary papaverine (48 +/- 25, 52 +/- 19 and 54 +/- 21 cm/s, respectively; all p less than 0.05 vs. baseline) and was significantly higher than in group 2 (37 +/- 24, 32 +/- 16, 41 +/- 23 cm/s; all p less than 0.05 vs. group 1). The coronary vasodilator reserve ratio (calculated as the ratio of hyperemic to basal mean flow velocity) for adenosine and papaverine was 2.94 +/- 1.50 and 2.94 +/- 1.00, respectively, in group 1 and was significantly and similarly reduced in group 2 (2.16 +/- 0.81 and 2.38 +/- 0.78, respectively; both p less than 0.05 vs. group 1). Low dose bolus injection of adenosine increased mean velocity equivalently to that after continuous infusion of 100 micrograms/kg, but less than after papaverine. There was a strong correlation between adenosine infusion and papaverine for both mean coronary flow velocity and coronary vasodilator reserve ratio (r2 = 0.871 and 0.325; SEE = 0.068 and 0.189, respectively; both p less than 0.0005). No patient had significant arrhythmias or prolongation of the corrected QT (QTc) interval with adenosine, but papaverine increased the QT (QTc) interval from 445 +/- 44 to 501 +/- 43 ms (p less than 0.001 vs. both maximal adenosine and baseline) and produced nonsustained ventricular tachycardia in one patient.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine↗
PubMed1991

The same CCAAT box-binding factor binds to the promoter of two coordinately regulated major histocompatibility complex class II genes.

Using competition mobility shift, methylation interference, and proteolytic clipping DNA binding assays, we demonstrate that the protein binding the major histocompatibility complex A beta CCAAT box is indistinguishable from the protein previously named NF-Y, which binds the major histocompatibility complex E alpha CCAAT box. Although the two CCAAT boxes share the same 10-base core sequence, termed the Y box, their flanking sequences, known to be important for binding, are very different.

Animals↗
PubMed1990

Rapid identification of the course of anomalous coronary arteries in adults: the "dot and eye" method.

It is often difficult to delineate the true course of anomalous coronary arteries by angiography because it only provides a 2-dimensional view of a complex 3-dimensional structure. The purpose of this study was to confirm morphologically the radiographic appearance of anomalous coronary arteries and to construct a protocol for rapid determination of their true course. Twenty-one adults who had anomalous origin of coronary arteries without other evidence of congenital heart disease were reviewed. Using an anatomically correct model of the heart, solder wire was placed in the pathologically described anomalous positions and radiographed. With this model the pathologically described courses could be easily recognized and separated radiographically. These courses were confirmed in the operating room in 2 patients and a rare anomaly of posterior origin of a coronary artery was also confirmed by autopsy.

Adult↗
PubMed1990

Relation of silent myocardial ischemia after coronary artery bypass grafting to angiographic completeness of revascularization and long-term prognosis.

The prevalence and characteristics of silent myocardial ischemia as detected by 24-hour ambulatory electrocardiography ST-segment depression were prospectively assessed in 94 patients examined early (1 to 3 months) and 184 patients examined late (12 months) after coronary artery bypass grafting (CABG), and followed for a mean of 48 +/- 11 (range 4 to 62) months. The relation of ambulatory electrocardiographic silent ischemia to evidence of completeness of revascularization as defined by cardiac angiography performed 1 and 12 months after CABG, and to prognosis by follow-up of adverse clinical events was analyzed. Silent ischemia was detected early in 20% (19 of 94) and late in 27% (50 of 184) of patients, and showed a mean frequency of episodes ranging from 6 to 10 episodes/24 hours with a mean duration ranging from 15 to 23 minutes. The circadian distribution of episodes disclosed a significant peak of ischemic activity during the period of 6 A.M. to noon and a secondary peak between 6 P.M. and midnight (p less than 0.01 and p less than 0.001, respectively). Silent ischemia was not found by univariate analysis to be associated with graft or anastomotic site occlusions, low graft flow rates, grafted arteries with significant distal residual stenoses or ungrafted stenotic native coronary arteries. Kaplan-Meier analysis of time to cardiac event showed that silent ischemia was not predictive of an adverse clinical event in the early years after CABG. Cox regression analysis of 30 covariates only disclosed age (relative risk 1.06 [95% confidence interval, 1.01 to 2.94]) as having an effect on time to adverse clinical event.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiography↗
PubMed1990

Ventricular arrhythmia due to intracoronary papaverine: analysis of QT intervals and coronary vasodilatory reserve.

Intracoronary papaverine commonly produces striking QT interval prolongation with rare but serious ventricular dysrhythmias reported. Because of 3 cases of severe papaverine-induced dysrhythmia in our laboratory, QT intervals and hemodynamic and intracoronary velocity data collected during intracoronary papaverine administration were retrospectively reviewed in 34 patients; 20 patients with angiographically normal coronary arteries (group 1) and 14 patients (group 2) before and (group 2) after single-vessel left coronary angioplasty. QT intervals increased from 394 +/- 44 to 464 +/- 73 msec, 414 +/- 47 to 504 +/- 95 msec, and 410 +/- 41 to 486 +/- 75 msec for groups 1 and 2 before and after angioplasty, respectively (all P less than 0.01). There was no correlation with hemodynamic, electrocardiographic, or coronary vasodilatory reserve responses and change in QTc interval. In the 3 index patients having significant papaverine-related arrhythmias, a baseline QT interval was prolonged (after prior papaverine exposure) in only 1 in association with torsade de pointes. These data indicate that QT interval prolongation after papaverine is a common occurrence, but that the production of ventricular dysrhythmia is probably idiosynchratic in origin. In view of these findings, we recommend that appropriate antiarrhythmic preparations be in place for patients receiving intracoronary papaverine.

Adult↗