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Biomedical subjects

M J Kern

Publications and source records attributed to M J Kern.

At least 307 records · Page 17Linked to original sources
PubMed1989

Emergency coronary artery bypass grafting for failed angioplasty: risk factors and outcome.

It has been suggested that coronary artery bypass grafting (CABG) performed in the setting of emergent failure of percutaneous transluminal coronary angioplasty causes minimal increased risk compared with routine CABG. We reviewed the records of 103 patients undergoing emergency CABG for failed percutaneous transluminal coronary angioplasty (group 1) and compared them with an identical number of consecutive CABG patients from 1987 (group 2). Group 1 had a lower risk profile evidenced by lower mean age (p less than 0.01), fewer diseased vessels (p less than 0.0001), better ventricular function (p less than 0.001), fewer left main lesions (p less than 0.0001), and fewer patients with acute ischemia requiring intravenous administration of nitroglycerin (p less than 0.01). Despite these differences, the group 1 patients had a higher mortality rate (11% versus 1%; p less than 0.01) and a higher rate of perioperative infarctions (new Q wave) (22% versus 6%; p less than 0.01). An analysis of risk factors was performed in the group 1 patients using 36 preoperative and operative variables. Multivariate analysis revealed that left ventricular score (p less than 0.0001), preoperative (after percutaneous transluminal coronary angioplasty) need for inotropic support (p less than 0.005), and age (p less than 0.025) were independent predictors of operative mortality. In conclusion, emergency CABG after failed percutaneous transluminal coronary angioplasty carries a significantly greater risk of operative death and perioperative infarction than elective CABG.

Angioplasty, Balloon↗
PubMed1989

Effects of pharmacologic coronary hyperemia on echocardiographic left ventricular function in patients with single vessel coronary artery disease.

To assess whether pharmacologic coronary vasodilation could provoke new left ventricular wall motion abnormalities in patients with single vessel coronary artery disease, systemic hemodynamics, coronary blood flow velocity and left ventricular wall motion were measured by two-dimensional echocardiography during administration of 10 mg of intracoronary papaverine in 14 patients before and again immediately after left coronary angioplasty (group 1). As a comparison with an intravenous method, left ventricular wall motion was analyzed after 0.56 mg/kg body weight of intravenous dipyridamole in a separate group of 13 patients with single vessel coronary disease (group 2). Heart rate-blood pressure product increased 3% to 6% in papaverine-treated patients and 14 +/- 11% (p = NS) in dipyridamole-treated patients. No angiographic collateral vessels were present in either group. Although intracoronary mean flow velocity measured in the 14 group 1 patients and in 5 normal control subjects during papaverine treatment increased from 125% to 400% of basal flow velocity, papaverine induced new left ventricular wall motion abnormalities in only 5 of the 14 patients before coronary angioplasty. In three of five patients, left ventricular wall motion abnormalities persisted after successful coronary angioplasty. Four of the 14 patients demonstrated augmentation of left ventricular wall motion with papaverine. After intravenous dipyridamole, only 3 of the 13 group 2 patients developed new left ventricular regional asynergy. These data suggest that selective (papaverine) and, most likely, global (dipyridamole) augmentation of coronary flow alone does not reliably identify potential ischemic left ventricular regions affected by critical single vessel coronary artery disease.

Angiography↗
PubMed1989

Left ventricular diastolic function: comparison of pulsed Doppler echocardiographic and hemodynamic indexes in subjects with and without coronary artery disease.

To evaluate the influence of left ventricular chamber stiffness and relaxation on Doppler echocardiographic indexes of diastolic function, 35 patients (mean age 60 +/- 12 years) were examined; 24 had coronary artery disease and 11 (Group I) had no cardiovascular disease. Micromanometer left ventricular pressure was recorded simultaneously with Doppler echocardiograms of mitral valve inflow and M-mode echocardiograms of left ventricular diameter. The chamber stiffness constant (k) was derived from the pressure-diameter relation. Relaxation was assessed by the isovolumic relaxation time constant (tau) derived from the exponential left ventricular pressure decay. The patients with coronary artery disease were classified into two groups on the basis of complete (Group II; n = 10) and incomplete (Group III; n = 14) relaxation. In Group I (no coronary disease), significant correlations were demonstrated between the chamber stiffness constant and the peak early filling velocity (r = 0.73; p less than 0.02), peak early to atrial filling velocity ratio (r = 0.82; p less than 0.005), atrial time-velocity integral (r = -0.73; p less than 0.02), early to atrial time-velocity integral ratio (r = 0.70; p less than 0.05), percent atrial contribution to filling (r = -0.64; p less than 0.05) and one-half filling fraction (r = 0.73; p less than 0.02). In Group II (coronary disease with complete relaxation), the chamber stiffness constant correlated with peak early filling velocity (r = 0.68; p less than 0.05), early filling time-velocity integral (r = 0.65; p less than 0.05) and early to atrial time-velocity integral ratio (r = 0.74; p less than 0.02). No correlations between k and Doppler indexes were found in Group III (coronary disease with incomplete relaxation). However, Group III demonstrated significant correlations between tau and the peak early filling velocity (r = -0.71; p less than 0.005), percent atrial contribution to filling (r = 0.56; p less than 0.05) and mean acceleration rate of early filling (r = -0.79; p less than 0.002). Thus, in subjects with normal relaxation, increasing chamber stiffness was associated with an enhanced peak early filling velocity and volume and decreased filling during atrial systole. This finding differs strikingly from the proposed influence of chamber stiffness on diastolic filling postulated by several researchers.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1989

Influence of alteration in preload on the pattern of left ventricular diastolic filling as assessed by Doppler echocardiography in humans.

We examined the influence of alterations in preload on pulsed Doppler indexes of left ventricular diastolic function in 50 patients including 12 without cardiovascular disease, 29 with coronary artery disease, and nine with critical aortic stenosis. Micromanometer left ventricular pressure was recorded simultaneously with pulsed Doppler echocardiography of left ventricular inflow and M-mode echocardiography of left ventricular diameter. Chamber stiffness constants, kd and kv, were obtained from the diastolic pressure-diameter and pressure-volume relations, respectively. Relaxation was measured by the isovolumic relaxation time constants, TL and TD, derived from the exponential left ventricular pressure decay and maximum negative dP/dt. In 41 patients after nitroglycerin treatment, left ventricular end-diastolic pressure decreased from 18 +/- 5 to 13 +/- 4 mm Hg (p less than 0.001). The ratio of peak early to peak atrial filling velocities and time-velocity integral ratios decreased from 1.08 +/- 0.57 to 0.90 +/- 0.42 (p less than 0.001) and from 1.77 +/- 0.95 to 1.41 +/- 0.71 (p less than 0.001), respectively. The peak early filling velocity and time-velocity integral decreased from 56.1 +/- 15.7 to 49.9 +/- 14.5 cm/sec (p less than 0.001) and from 7.9 +/- 2.7 to 6.8 +/- 2.8 cm (p less than 0.001), respectively. Relaxation (TL, TD, and maximum negative dP/dt) and chamber stiffness (kd and kv) were not impaired after nitroglycerin administration. In 48 patients after ventriculography, left ventricular end-diastolic pressure increased from 18 +/- 6 to 22 +/- 8 mm Hg (p less than 0.001). The peak early and peak atrial filling velocities increased from 57.4 +/- 15.2 to 68.3 +/- 19.7 cm/sec (p less than 0.001) and from 61.0 +/- 22.7 to 69.4 +/- 23.2 cm/sec (p less than 0.01), respectively. As a result, the ratio of peak early to peak atrial filling velocity was unchanged. However, in the aortic stenosis group, the ratio of peak early to peak atrial filling velocity increased from 0.95 +/- 0.64 to 1.10 +/- 0.72 (p less than 0.02). Relaxation and chamber stiffness were unchanged. Thus, a reduction or increase in preload may induce a diastolic filling pattern that mimics or masks diastolic dysfunction, respectively. Preload conditions need to be accounted for when the status of diastolic function is extrapolated from the pulsed Doppler mitral inflow velocity profile.

Aortic Valve Stenosis↗
PubMed1989

Influence of calcium channel antagonist therapy on the ischemic response to acute coronary occlusion in humans.

The effects of calcium channel blockers on myocardial ischemia in humans can be evaluated in studies reporting changes during coronary angioplasty. These studies indicate that the extent and duration of myocardial ischemia in most patients with single vessel coronary artery disease can be improved somewhat by calcium channel blockers. The anti-ischemic effects of intravenous diltiazem, nifedipine, nisoldipine, and nicardipine are discussed. Intravenous diltiazem produces effects similar to intracoronary, but not systemic, nifedipine. Intracoronary nifedipine and nicardipine produce similar degrees of cardioplegia in most studies. Nicardipine and nisoldipine also reduce signs of myocardial ischemia, although different mechanisms are postulated to be involved. Although clinically beneficial in some patients, data indicate that the cardioprotective effect of calcium channel blockers during supply-side ischemia is less potent than reperfusion with blood. For the most part, calcium channel antagonists function through reduction of myocardial oxygen demand with rare agents favorably influencing collateral flow or providing direct myocardial protection. The potential myocardial cellular effects of calcium channel blockers on supply-side ischemia merit further investigation.

Acute Disease↗
PubMed1988

Increased frequency of restenosis in patients continuing to smoke cigarettes after percutaneous transluminal coronary angioplasty.

The influence of continued cigarette smoking on restenosis after percutaneous transluminal coronary angioplasty (PTCA) was retrospectively determined through a study of 160 patients with primary success who underwent follow-up angiography after a mean of 7 +/- 7 months. The average number of narrowings at risk for restenosis was 1.7/patient in the 84 patients who continued to smoke (group 1) and 1.9/patient in the 76 patients who stopped smoking at the time of PTCA (group 2) (difference not significant). The 2 patient groups at baseline were similar with respect to gender, frequency of diabetes mellitus, number of pack/year smoking, angina class and number of diseased coronary arteries. The location of the dilated narrowings, the residual luminal diameter stenosis and the transstenotic gradient after the procedure were similar in both groups. The recurrence of angina greater than or equal to class II was the reason for restudy in 43% and 36% of group 1 and group 2 patients, respectively. Restenosis, defined as the presence of greater than or equal to 50% narrowing at the site of previous successful dilatation at follow-up angiography, was significantly higher in group 1 compared with group 2 patients (55% vs 38%, p = 0.03). Continued smoking was selected as an independent predictor of restenosis by logistic regression analysis. The incidence of coronary artery disease progression (14% vs 10%) was not significantly different between the 2 groups. In conclusion, continued smoking after successful PTCA is associated with an increased risk of restenosis. The higher restenosis rate in smokers emphasizes the need to strengthen educational programs after PTCA.

Angioplasty, Balloon↗
PubMed1988

Nitroglycerin-induced coronary vasodilatory responses in patients during isometric handgrip exercise.

Intracoronary nitroglycerin is frequently administered during invasive procedures such as coronary angioplasty or thrombolysis which may be associated with pain and sympathetic neural stimulation. Whether sympathetic-mediated reflex vasoconstriction interferes with nitroglycerin-induced augmentation of coronary blood flow is unknown. Therefore, coronary and systemic hemodynamics were measured in 19 patients during isometric handgrip exercise (3 min x 25% maximal effort), during intracoronary nitroglycerin, and during handgrip plus intracoronary nitroglycerin. Nine patients had no significant left anterior descending coronary artery stenosis (group 1) and ten patients had greater than 70% left anterior descending coronary artery stenosis (group 2). Handgrip exercise increased heart rate, mean arterial pressure, and coronary sinus and great vein flow 15% while increasing coronary resistance 10%. Intracoronary nitroglycerin (200 micrograms) reduced mean arterial pressure -4 +/- 6% and increased great cardiac vein flow 35-72%. Anterior left ventricular regional coronary flow responses to intracoronary nitroglycerin were unaffected by sympathetic stimulation for group 1. Group 2 had a greater increase in great vein flow with intracoronary nitroglycerin plus handgrip compared to nitroglycerin alone due to increased mean arterial pressure with no change in the great vein resistance. These data indicate that sympathetic stimulation does not alter the nitroglycerin-induced augmentation of coronary sinus and great vein blood flow in patients with and without significant left anterior descending coronary artery stenosis. In patients undergoing invasive interventions who may have increased circulating catecholamines, mild sympathetic (isometric) stimulation does not appear to interfere with the coronary vasodilatory responses to intracoronary nitroglycerin.

Cardiac Catheterization↗
PubMed1988

Percutaneous brachial catheterization: the hidden hazard of high brachial artery bifurcation.

We describe a patient in whom a brachial arterial cutdown done at the same site for percutaneous transluminal angioplasty immediately after uncomplicated percutaneous brachial coronary arteriography revealed the percutaneous sheath in a deeper, smaller, and more lateral artery than the brachial artery, complicating placement of the guiding catheter. This case illustrates the potential hidden hazard of normal brachial artery bifurcation variants, which may be responsible for some of the potential complications encountered in percutaneous brachial artery catheterization techniques.

Aged↗
PubMed1988

Percutaneous balloon valvuloplasty and coronary angioplasty for the treatment of calcific aortic stenosis and obstructive coronary artery disease in an elderly patient.

An 81-year-old man with severe calcific aortic stenosis and coronary artery disease who refused surgical therapy was treated with sequential percutaneous balloon aortic valvuloplasty (PBAV) and percutaneous transluminal angioplasty. Before percutaneous balloon valvuloplasty, the mean aortic gradient was 76 mmHg, and the aortic valve area was .45 cm2. The aortic valve was dilated using 15-mm and 18-mm balloons. The mean gradient decreased to 40 mmHG, and the aortic valve area increased to .62 cm2. Percutaneous transluminal coronary angioplasty (PTCA) was performed 2 weeks later, and an 85% proximal left circumflex stenosis was successfully dilated to 20%. No complications were noted during either procedure. At 6-month follow-up, the patient had returned to normal activities and was asymptomatic. Thus, combined therapy with PBAV and PTCA is technically feasible in selected elderly patients with calcific aortic stenosis and anatomically suitable coronary artery disease. This nonsurgical therapeutic approach may be useful in the treatment of selected patients who refuse or who are deferred from cardiac surgery.

Aged↗
PubMed1988

Effects of beta-adrenergic blockade on nitroglycerin-induced augmentation of regional coronary blood flow in patients.

Although beta-adrenergic blockade may increase coronary vascular resistance in some patients with severe ischemic heart disease, the effects of beta blockade on the nitroglycerin (NTG)-induced augmentation of coronary blood flow have not been elucidated. Therefore, systemic hemodynamic and anterior left ventricular regional coronary blood-flow (thermodilution) data were measured during administration of NTG into the left coronary artery, before and 10 min after intravenous propranolol (0.1 mg/kg) in 22 patients. Six patients (Group 1) had normal left coronary arteries and nine (Group 2) had severe coronary artery disease with at least greater than 70% narrowing of the left anterior descending artery. In seven additional patients (three without and four with greater than 70% left anterior descending coronary artery disease), measurements were obtained with constant-paced heart rates (Group 3). Before beta blockade, NTG (200 mcg) significantly increased anterior regional great-vein flow [for Group 1, 84 +/- 38% (81 +/- 20 to 140 +/- 60 ml/min); Group 2, 39 +/- 41% (61 +/- 26 to 83 +/- 38 ml/min); and Group 3, 87 +/- 55% (75 +/- 36 to 144 +/- 86 ml/min)]. In Groups 1 and 2, beta-adrenergic blockade reduced heart rate 10% (p less than 0.01) but did not affect mean arterial or pulmonary artery pressures.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1988

Acute myocardial infarction during percutaneous aortic balloon valvuloplasty.

Balloon valvuloplasty has been shown to be a relatively safe and effective intervention in palliating the symptoms of severe calcific aortic stenosis in the elderly [1-7]. Although the mechanism of balloon valvuloplasty is plastic deformation and fracture of the calcified valve tissue [2], complications such as embolic events or acute myocardial infarction due to aortic balloon valvuloplasty are very rare. Previously published reports mentioned only one case of cerebral embolism [5] and two patients with late fatal myocardial infarction [4]. In this report we present an elderly patient with calcific aortic stenosis who developed an acute lateral myocardial infarction during percutaneous balloon aortic valvuloplasty.

Aged↗
PubMed1988

Effects of nitroglycerin and nifedipine on coronary and systemic hemodynamics during transient coronary artery occlusion.

Nitroglycerin (NTG) and nifedipine (NIF) have the potential to augment coronary blood flow in addition to reducing peripheral determinants of myocardial oxygen demand as a synergistic protective mechanism during ischemia. To examine these effects, systemic and coronary hemodynamic responses were measured continuously before and during brief periods of myocardial ischemia induced by left anterior descending coronary balloon occlusion in 26 patients undergoing angioplasty (PTCA). Data were compared for two matched occlusion periods, one control and one "drug" occlusion. In 17 patients (NTG group), 200 micrograms of intracoronary NTG was given immediately before coronary occlusion. In nine patients (NIF group), 10 mg of sublingual NIF was given 15 minutes before the "drug" occlusion. NTG significantly but transiently reduced mean arterial pressure (91 +/- 11 to 82 +/- 15 mm Hg, p less than 0.05) and augmented basal coronary blood flow (95 +/- 38 to 127 +/- 54 ml/min, p less than 0.05) but did not alter great vein blood flow (59 +/- 29 vs 61 +/- 29 ml/min) or coronary occlusion pressure (25 +/- 7 to 24 +/- 7 mm Hg) during ischemia. NIF significantly reduced systolic, diastolic, and mean arterial pressure (119 +/- 21 to 95 +/- 8 mm Hg, p less than 0.001) and heart rate-pressure product from control. NIF maintained basal great vein blood flow (125 +/- 41 to 106 +/- 57 ml/min) during reduced myocardial oxygen demand, but did not affect great vein blood flow (73 +/- 29 to 79 +/- 37 ml/min) or coronary occlusion pressures during ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Acute coronary occlusion occurring after successful percutaneous transluminal coronary angioplasty: temporal relationship to discontinuation of anticoagulation.

The incidence and prognosis of acute coronary reocclusion occurring after patients had left the catheterization laboratory following a successful percutaneous transluminal coronary angioplasty (PTCA) procedure and the temporal relation of this event to the discontinuation of systemic heparin administration were analyzed in a series of 1238 consecutive patients. Acute reocclusion, 1 to 96 hours after successful PTCA, occurred in 22 of 1238 patients (1.8%). Patients undergoing PTCA in the setting of acute myocardial infarction were excluded. Out of 22 patients, 15 had a nonocclusive dissection and four had evidence of small intracoronary thrombus immediately post-PTCA, with no evidence of flow disturbance. Acute reocclusion occurred within 5 hours of heparin discontinuation in 12 patients or while they were receiving inadequate anticoagulation (four patients). In 16 of 22 (73%) patients, acute reocclusion was temporally related to a time of diminished anticoagulation. Redilation was attempted in 14 patients and was ultimately successful in five patients (36%). Ten patients required coronary artery bypass surgery and three patients died. Our findings suggest that acute reocclusion after an initially successful PTCA has a poor outcome and seems to be temporally related to the loss of effective anticoagulation in most of these patients. It is advisable to discontinue heparin infusion at a time when facilities for urgent revascularization are available.

Acute Disease↗