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Biomedical subjects

M J Kern

Publications and source records attributed to M J Kern.

At least 343 records · Page 19Linked to original sources
PubMed1986

Dose-related effects of intracoronary nitroglycerin on coronary hyperemia in patients with coronary artery disease.

Although intracoronary nitroglycerin (NTG) is frequently required during percutaneous transluminal coronary angioplasty or thrombolysis, the dose-related hemodynamic effects and the extent to which intracoronary NTG--induced coronary hyperemia is limited in patients with coronary artery disease have not been defined. Therefore, we studied 19 patients with coronary artery disease (nine with no or minimal luminal narrowing of the left anterior descending coronary artery [group 1] and 10 with significant left anterior descending coronary stenosis [group 2]; mean arterial pressure and thermodilution coronary sinus and great cardiac vein blood flow were measured during bolus administrations of 50, 200, and 300 micrograms of intracoronary NTG. During the NTG-induced hyperemia, mean arterial pressure decreased 0%, 4% (both p = NS), and 6% (p less than 0.05) after 50, 200, and 300 micrograms doses, respectively. heart rate did not change. Global coronary hyperemia was greatest for 200 micrograms with coronary blood flow increasing (74 +/- 32% in group 1 and 53 +/- 25% for group 2) but was significantly different from 50 micrograms only in group 2 patients. Moreover, the regional coronary blood flow responses were attenuated in group 2 compared to group 1 for 50 micrograms, 18 +/- 13% vs 38 +/- 18%, and for 200 micrograms, 35 +/- 15% vs 72 +/- 34% (both p less than 0.05), with the reduction of regional coronary resistance in group 2 attenuated for all three doses of intracoronary NTG. The 300 micrograms dose did not provide further augmentation of either global or regional coronary blood flow or greater reduction in coronary resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1986

Quantitative evaluation of aortic insufficiency by continuous wave Doppler echocardiography.

To assess the usefulness of continuous wave Doppler echocardiography in the evaluation of aortic insufficiency, the aortic regurgitant flow velocity pattern obtained with continuous wave Doppler examination was compared with the results of aortography and conventional pulsed Doppler techniques in 25 individuals with aortic insufficiency. The diastolic deceleration slope as measured from the continuous wave tracing was significantly different among subgroups of patients with mild (1.6 +/- 0.5 m/s2), moderate (2.7 +/- 0.5 m/s2) and severe (4.7 +/- 1.5 m/s2) aortic insufficiency as determined from aortography. Deceleration slopes greater than 2 m/s2 separated individuals with moderate and severe insufficiency from those with mild insufficiency. Similar findings were seen when comparing the pressure half-time method of diastolic velocity decay with the more severe grades of aortic insufficiency exhibiting the shortest pressure half-times. There was also a high correlation (r = 0.85) between the deceleration slope measured by continuous wave Doppler recordings and the grade of insufficiency as assessed by pulsed Doppler echocardiography. End-diastolic velocities correlated poorly (r = 0.28) with catheter-measured end-diastolic pressure difference between the aorta and the left ventricle. These findings demonstrate that the aortic regurgitant flow pattern by continuous wave Doppler echocardiography may be useful in quantitating the degree of aortic insufficiency by assessing the rate with which aortic and left ventricular pressures equilibrate during diastole.

Adult↗
PubMed1986

Alteration of "jetlike" laminar flow after percutaneous transluminal angioplasty of saphenous vein bypass graft stenosis.

Coronary angiography in a patient with a stenosis in a saphenous vein graft 7 years after surgical anastomosis demonstrated a striking angiographic "jetlike" laminar flow pattern. Both the severe stenosis and "jet" appearance were markedly altered after percutaneous transluminal coronary angioplasty (PTCA). We believe this unusual angiographic finding represents visual evidence of a pressure gradient and severe disturbance of laminar flow across the lesion, which was improved after PTCA.

Adult↗
PubMed1985

Improved myocardial oxygen utilization by diltiazem in patients.

Calcium entry blocking drugs produce different effects on systemic and coronary hemodynamics and myocardial oxygen extraction. To examine the effects on myocardial oxygen extraction, intravenous diltiazem (100 micrograms/kg bolus with a continuous 10 micrograms/kg/min infusion) was administered to 11 patients at rest and during controlled heart rates (100 +/- 5 and 120 +/- 5 bpm). At rest, diltiazem decreased mean arterial pressure from 109 +/- 13 to 99 +/- 14 mm Hg (p less than 0.01), increased heart rate from 64 + 12 to 74 +/- 14 bpm (p less than 0.01), and decreased coronary sinus resistance (1.02 +/- .41 to 0.87 +/- .40 U, p less than 0.05). Myocardial oxygen extraction was significantly reduced since coronary sinus oxygen content increased (6.0 +/- 0.9 to 7.8 +/- 1.2 ml/dl, p less than 0.01) and the arterial-coronary sinus oxygen difference decreased (12.0 +/- 1.7 to 10.6 +/- 1.6 ml/dl, p less than 0.01). Similar changes occurred with heart rate held constant. There were no significant changes in absolute coronary sinus blood flow, calculated myocardial oxygen consumption, or left ventricular dP/dt. Diltiazem decreases mean arterial pressure while reducing both myocardial oxygen extraction and coronary arterial resistance, suggesting that a principal mechanism of a beneficial effect upon the coronary circulation appears to be an improvement in myocardial oxygen extraction relative to myocardial oxygen demand.

Adult↗
PubMed1985

Effects of pulsed external augmentation of diastolic pressure on coronary and systemic hemodynamics in patients with coronary artery disease.

The purpose of this study was to define the effects of pulsed external diastolic pressure augmentation on coronary and systemic hemodynamics in 14 men with coronary artery disease and normal left ventricular function. Coronary sinus and great vein blood flow (thermodilution) and systemic hemodynamics were measured before, during, and after timed lower extremity compression, augmenting peak diastolic pressure to within 5 mm Hg of systolic pressure. Systolic and diastolic pressure-time indices were calculated from the high-fidelity micromanometer left ventricular-aortic recordings. External counterpulsation increased mean arterial pressure (108 +/- 11 [1 SD] to 114 +/- 12 mm Hg, p less than 0.01) and the diastolic pressure-time index (440 +/- 51 to 498 +/- 82 units, p less than 0.01), with no change in the systolic pressure-time index, absolute coronary sinus, or great cardiac vein blood flow. External diastolic pressure augmentation did not affect heart rate, right heart hemodynamics, cardiac output, or calculated myocardial oxygen consumption. An unanticipated finding was a greater than or equal to 10% reduction in peak systolic pressure during external diastolic pressure augmentation in 8 of 14 patients. Despite minimal changes in absolute myocardial blood flow and oxygen consumption, the increase in the diastolic pressure-time/systolic pressure-time index ratio suggests that subendocardial perfusion may be favorably influenced by diastolic pressure augmentation and may explain the previously reported clinical benefits of external counterpulsation in some patients with ischemic heart disease.

Adult↗
PubMed1985

Regional coronary vasoconstriction after combined beta-adrenergic and calcium channel blockade in patients with coronary artery disease.

The beta-adrenergic and calcium channel blocking drugs, which individually and combined have proven efficacious in the treatment of angina pectoris, appear to have opposing effects on coronary artery vasomotion. Previous studies have shown that beta-adrenergic blockade may potentiate and calcium channel blockade reverse coronary vasoconstriction during adrenergic cold stimulation in patients with coronary artery disease. To assess the coronary hemodynamic effects of combined drug therapy, thermodilution coronary sinus and great cardiac vein flow and mean arterial pressure were measured during serial cold pressor testing, both before and after 0.1 mg/kg of intravenous propranolol and again after the addition of 10 mg of sublingual nifedipine in 21 patients (9 without [group A1] and 12 with [group A2] greater than 50% narrowing of the left anterior descending coronary artery). In an additional 15 patients (6 patients without [group B1] and 9 with [group B2] left anterior descending artery stenosis), serial cold pressor testing was performed reversing the drug order. Despite significant increases in mean arterial pressure (p less than 0.01) during cold pressor testing, coronary sinus resistance responses after propranolol plus nifedipine were not statistically significant for any group. However, regional coronary resistance responses differed between patients with and without left anterior descending artery stenosis. In group A1, great cardiac vein resistance was unchanged after propranolol plus nifedipine. In group A2, great cardiac vein flow decreased significantly after propranolol plus nifedipine from 8 +/- 17 to -4 +/- 12% (p less than 0.01 versus control), and great cardiac vein resistance increased from 4 +/- 21 to 15 +/- 19% (p less than 0.01 versus control). A similar significant response was observed for groups B1 and B2. Regional coronary vasoconstriction during adrenergic stimulation after combined drug therapy was only observed in patients with significant left anterior descending artery stenosis. These data suggest that in some patients with severe coronary artery disease, combined beta-adrenergic and calcium channel blockade modified regional coronary responses to adrenergic stimulation with an inhomogeneous distribution of blood flow to potentially ischemic regions without affecting total coronary blood flow. These data also imply that an improvement in anginal symptoms after combined drug therapy may be due primarily to mechanisms that reduce myocardial oxygen demand rather than to improved myocardial oxygen supply.

Adrenergic beta-Antagonists↗
PubMed1985

Attenuation of coronary vascular resistance by selective alpha 1-adrenergic blockade in patients with coronary artery disease.

Alpha-adrenergic-mediated coronary vasoconstriction during stress such as cold pressor testing may contribute to myocardial ischemia by increasing coronary vascular resistance in patients with severe coronary artery disease. Nonselective alpha-receptor blockade with phentolamine abolishes both the peripheral and coronary vasoconstriction during cold pressor testing, but causes reflex tachycardia and increased inotropy. To determine the role of selective alpha 1-receptor blockade, the changes in coronary vascular resistance during cold pressor testing were measured in 18 patients with coronary artery disease before and after intravenous administration of 100 mg of trimazosin. Cold pressor testing was performed at a constant paced subanginal heart rate of 95 +/- 5 beats/min (+/- 1 SD). Before trimazosin, cold pressor testing increased mean arterial pressure by 9 +/- 4% (102 +/- 14 to 111 +/- 14 mm Hg, p less than 0.001) with no change in coronary sinus blood flow, but significantly increased coronary vascular resistance by 15 +/- 19% (1.02 +/- 0.46 to 1.15 +/- 0.57 units, p less than 0.05). Five minutes after trimazosin, cold pressor testing increased mean arterial pressure by 6 +/- 5% (p less than 0.001) with a marked attenuation of the increase in coronary vascular resistance (6 +/- 11%, p = NS), which was significantly less than before trimazosin (p less than 0.02). Trimazosin did not increase plasma norepinephrine concentration at rest, suggesting that in the dosage used trimazosin caused selective alpha 1-receptor blockade.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1983

Angioplasty catheter communication mimicking coronary arterial dissection.

We report a case in which a sudden communication between the pressure and balloon inflation lumens of a percutaneous transluminal angioplasty (PTCA) catheter angiographically mimicked dissection of the coronary artery. This case illustrates a previously undescribed catheter artifact that must be differentiated from other complications of PTCA.

Aortic Dissection↗
PubMed1983

Potentiation of coronary vasoconstriction by beta-adrenergic blockade in patients with coronary artery disease.

Although beta-adrenergic blocking agents reduce myocardial oxygen consumption and symptoms of myocardial ischemia in patients with coronary artery disease (CAD), propranolol has been reported to exacerbate coronary artery spasm in some patients with variant angina. To determine whether increased coronary vasomotor tone can be induced by beta-adrenergic blockade, we measured the changes in coronary vascular resistance (CVR) during cold pressor testing (CPT) in 15 patients, nine with severe CAD and six with normal left coronary anatomy, before and after i.v. propranolol (0.1 mg/kg). Coronary blood flow was measured by coronary sinus thermodilution. CVR was calculated as mean arterial pressure divided by coronary sinus blood flow. Heart rate was maintained constant at a paced subanginal rate of 95 +/- 5 beats/min. Before propranolol, CPT induced significant increases in coronary vascular resistance in patients with CAD (15.0 +/- 2.2%, p less than 0.02), but no increase in CVR in the normal patients. After propranolol, the CVR change during CPT was augmented for patients with CAD (29 +/- 6%, p less than 0.01) and for the normal population (9 +/- 5%, NS). The potentiated increase in CVR occurred without significant changes in resting CVR or in the magnitude of the hypertensive response to CPT. We conclude that beta-adrenergic blockade with propranolol can potentiate coronary artery vasoconstriction in some patients with CAD, possibly mediated by unopposed alpha-adrenergic vasomotor tone. These changes may be important in patients in whom intense adrenergic stimulation may increase coronary artery tone and adversely influence the balance between myocardial oxygen supply and demand.

Adrenergic beta-Antagonists↗