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G R Heyndrickx

Publications and source records attributed to G R Heyndrickx.

At least 55 records · Page 3Linked to original sources
PubMed1993

Luminal narrowing after percutaneous transluminal coronary angioplasty. A study of clinical, procedural, and lesional factors related to long-term angiographic outcome. Coronary Artery Restenosis Prevention on Repeated Thromboxane Antagonism (CARPORT) Study Group.

BACKGROUND: The renarrowing process after successful percutaneous transluminal coronary angioplasty (PTCA) is now believed to be caused by a response-to-injury vessel wall reaction. The magnitude of this process can be assessed by the change in minimal lumen diameter (MLD) at follow-up angiography. The aim of the present study was to find independent patient-related, lesion-related, and procedure-related risk factors for this luminal narrowing process. A model that accurately predicts the amount of luminal narrowing could be an aid in patient or lesion selection for the procedure, and it could improve assessment of medium-term (6 months) prognosis. Modification or control of the identified risk factors could reduce overall restenosis rates, and it could assist in the selection of patients at risk for a large loss in lumen diameter. This population could then constitute the target population for pharmacological intervention studies. METHODS AND RESULTS: Quantitative angiography was performed on 666 successfully dilated lesions at angioplasty and at 6-month follow-up. Multivariate linear regression analysis was performed to obtain variables with an independent contribution to the prediction of the absolute change in minimal lumen diameter. Diabetes mellitus, duration of angina < 2.3 months, gain in MLD at angioplasty, pre-PTCA MLD, lesion length > or = 6.8 mm, and thrombus after PTCA were independently predictive of change in MLD. Overall prediction of the model was poor, however, percentage-correct classification for a predicted change between -0.1 to -0.4 mm was approximately 10%. Lesions showing no change or regression (change > -0.1 mm) and lesions showing large progression (< or = -0.4 mm) were more predictable (correct classification, 59.5% and 49.7%, respectively). CONCLUSIONS: Renarrowing after successful PTCA as determined with contrast angiography is a process that cannot be accurately predicted by simple clinical, morphological, and lesion characteristics.

Angioplasty, Balloon, Coronary↗
PubMed1993

Evaluation of ketanserin in the prevention of restenosis after percutaneous transluminal coronary angioplasty. A multicenter randomized double-blind placebo-controlled trial.

BACKGROUND: Ketanserin is a serotonin S2-receptor antagonist that inhibits the platelet activation and vasoconstriction induced by serotonin and also inhibits the mitogenic effect of serotonin on vascular smooth muscle cells. METHODS AND RESULTS: We conducted a randomized, double blind, placebo-controlled trial to assess the effect of ketanserin in restenosis prevention after percutaneous transluminal coronary angioplasty (PTCA). Patients received either ketanserin (loading dose, 40 mg 1 hour before PTCA; maintenance dose, 40 mg bid for 6 months) or matched placebo. In addition, all patients received aspirin for 6 months. Coronary angiograms before PTCA, after PTCA, and at 6 months were quantitatively analyzed. Six hundred fifty-eight patients were entered into the intention-to-treat analysis. The primary clinical end point of the study was the occurrence between PTCA and 6 months of any one of the following: cardiac death, myocardial infarction, the need for repeat angioplasty, or bypass surgery. It also included the need for revascularization actuated by findings at 6-month follow-up angiography. The primary clinical end point was reached by 92 (28%) patients in the ketanserin group and 104 (32%) in the placebo group (RR, 0.89; 95% CI, 0.70, 1.13; P = .38). Quantitative angiography after PTCA and at follow-up was available in 592 patients (ketanserin, 287; control, 305). The mean difference in minimal lumen diameter between post-PTCA and follow-up angiogram (primary angiographic end point) was 0.27 +/- 0.49 mm in the ketanserin group and 0.24 +/- 0.52 mm in the control group (difference, 0.03 mm; 95% CI, -0.05, 0.11; P = .50). CONCLUSIONS: Ketanserin at the dose administered in this trial failed to reduce the loss in minimal lumen diameter during follow-up after PTCA and did not significantly improve the clinical outcome.

Adult↗
PubMed1993

Safety and efficacy of recombinant hirudin (CGP 39 393) versus heparin in patients with stable angina undergoing coronary angioplasty.

BACKGROUND: Enhanced thrombin activity has been associated with acute and long-term complications following balloon angioplasty (percutaneous transluminal coronary angioplasty (PTCA). We evaluated, in a 2-to-1 randomized, double-blind trial, the effects of recombinant hirudin, CGP 39 393, relative to unfractionated sodium heparin on periprocedural events, bleeding, early angiographic outcome, and coagulation in 113 patients with stable angina undergoing PTCA. METHODS AND RESULTS: Prior to PTCA, 20 mg CGP 39 393 was administered as a bolus, followed by continuous infusion at a rate of 0.16 mg.kg-1 x h-1, or 10,000 IU sodium heparin was administered as a bolus and continued at a rate of 12 IU.kg-1 x h-1 for 24 hours. Infusion was adjusted to activated partial thromboplastin time (APTT) levels. ST segment was monitored for 24 hours, and angiograms were analyzed with quantitative technique (QCA). In 74 CGP 39 393- and 39 heparin-treated patients, 132 lesions were dilated. Myocardial infarction and/or emergency coronary bypass surgery occurred in 1 (1.4%) CGP 39 393 patient compared with 4 (10.3%) heparin patients (relative risk, 7.6; 95% confidence interval, 0.9, 65.6). At 24 hours, complete perfusion was present in 91% heparin and 100% CGP 39 393 patients. Significant ST segment displacement was found in 11% of heparin versus 4% of CGP 39 393 subjects. Bleeding occurred only at the puncture site in 4 CGP 39 393-treated patients. QCA did not reveal significant differences between the groups. APTT values were more often in the target range and more stable in CGP 39 393 patients. Levels of thrombin-antithrombin III complexes, prothrombin fragment F1+2, and fibrinopeptide A indicated that CGP 39 393 was an effective inhibitor of thrombin activity. CONCLUSIONS: CGP 39 393 can safely be administered to patients undergoing elective PTCA for stable anginal symptoms and may have a more favorable anticoagulant profile than heparin.

Aged↗
PubMed1993

Recovery of regional contractile function and oxidative metabolism in stunned myocardium induced by 1-hour circumflex coronary artery stenosis in chronically instrumented dogs.

Stunned myocardium produced by 1 hour of critical coronary artery stenosis was evaluated for alteration in regional mechanical function and overall oxidative and fatty acid metabolism by positron emission tomography (PET) in chronically instrumented dogs. Twenty-seven dogs, chronically instrumented for measurements of left ventricular pressure and regional myocardial wall thickening in normal and ischemic zones, were subjected to a 1-hour period of myocardial ischemia produced by graded left circumflex coronary artery stenosis, resulting in minimal residual flow. Mean transmural myocardial flow during 1-hour coronary stenosis decreased to 0.34 +/- 0.04 ml/min per gram in the ischemic zones (normal zone transmural flow, 0.96 +/- 0.10 ml/min per gram). Systolic wall thickening in the ischemic zone was almost completely abolished (-97 +/- 4%). On reperfusion, systolic wall thickening immediately resumed but remained depressed. Progressive recovery was noted with time. At 24 hours, systolic wall thickening was still depressed (-20 +/- 6%, p < 0.01). At 1 week, wall thickening had completely recovered and was no longer significantly different from the control condition. In addition, the absence of necrosis at the site of wall thickness measurements was confirmed at autopsy in all dogs. No abnormalities were found by electron microscopy in four dogs undergoing myocardial biopsies at the time of PET studies. Dynamic PET studies using [1-11C]acetate tracer (performed at 6 hours, 1 week, and 2 weeks after reperfusion) and [1-11C]palmitic acid tracer (performed at 6 hours, 12 hours, 24 hours, 1 week, and 2 weeks after reperfusion) allowed the computation of regional tissue time-activity curves in different regions of interest at different times during follow-up. Despite full reperfusion, abnormal [1-11C]acetate and [1-11C]palmitic acid kinetics were observed in the posterior segments, previously subjected to ischemia, as evidenced by a significant decrease in the slope of the early 11C clearance curve component. Repeat PET studies revealed progressive normalization of overall oxidative metabolism and fatty acid metabolism, which paralleled the time course of recovery of mechanical function. Thus, myocardial ischemia, produced by 1-hour coronary artery stenosis, followed by full reperfusion is associated with a prolonged period of postischemic mechanical and metabolic dysfunction. This transient reduction in oxygen delivery induced a prolonged impairment in fatty acid beta-oxidation as well as a reduction in overall oxidative metabolism despite full reoxygenation. A similar time course for recovery of function and metabolism was observed.

Acetates↗
PubMed1991

Orifice variability of the stenotic aortic valve: evaluation before and after balloon aortic valvuloplasty.

The effects of balloon aortic valvuloplasty on orifice variability of the stenotic sclerocalcific aortic valve were evaluated by hemodynamic measurements of aortic valve function in 14 patients before balloon aortic valvuloplasty, during nitroprusside infusion before valvuloplasty, 48 h after valvuloplasty and during nitroprusside infusion 48 h after valvuloplasty. Aortic valve function was assessed by aortic valve area calculations with use of the Gorlin and Cannon formulas. Nitroprusside infusion before balloon aortic valvuloplasty caused no change in mean aortic valve gradient but a significant increase in mean aortic transvalvular flow from 186 +/- 46 to 202 +/- 61 ml/s (p less than 0.05), in Gorlin aortic valve area from 0.49 +/- 0.17 to 0.53 +/- 0.21 cm2 (p less than 0.05) and in Cannon aortic valve area from 0.45 +/- 0.18 to 0.49 +/- 0.22 cm2 (p less than 0.05). Nitroprusside infusion 48 h after valvuloplasty induced no change in mean aortic valve gradient but a significant increase in mean aortic transvalvular flow from 214 +/- 61 to 254 +/- 78 ml/s (p less than 0.005), in Gorlin aortic valve area from 0.71 +/- 0.25 to 0.83 +/- 0.32 cm2 (p less than 0.01) and in Cannon aortic valve area from 0.78 +/- 0.33 to 0.88 +/- 0.40 cm2 (p less than 0.05). Forty-eight hours after valvuloplasty, nitroprusside infusion induced a larger increase (40 +/- 40 ml/s) in mean transvalvular flow than before valvuloplasty (16 +/- 27 ml/s; p less than 0.05) and a larger increase (0.12 +/- 0.14 cm2) in Gorlin aortic valve area than before valvuloplasty (0.05 +/- 0.07 cm2; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1991

Prevention of restenosis after percutaneous transluminal coronary angioplasty with thromboxane A2-receptor blockade. A randomized, double-blind, placebo-controlled trial. Coronary Artery Restenosis Prevention on Repeated Thromboxane-Antagonism Study (CARPORT).

BACKGROUND: GR32191B is a novel thromboxane A2-receptor antagonist with potent antiagregational and antivasoconstrictive properties. We have conducted a randomized, double-blind placebo-controlled trial to study its usefulness in restenosis prevention. METHODS AND RESULTS: Patients received either GR32191B (80 mg orally before angioplasty and 80 mg/day orally for 6 months) or 250 mg i.v. aspirin before angioplasty and placebo for 6 months. Coronary angiograms before angioplasty, after angioplasty, and at 6-month follow-up were quantitatively analyzed. Angioplasty was attempted in 697 patients. For efficacy analysis, quantitative angiography at follow-up was available in 522 compliant patients (261 in each group). Baseline clinical and angiographic parameters did not differ between the two treatment groups. The mean difference in coronary diameter between postangioplasty and follow-up angiogram (primary end point) was -0.31 +/- 0.54 mm in the control group and -0.31 +/- 0.55 mm in the GR32191B group. Clinical events during 6-month follow-up, analyzed on intention-to-treat basis, were ranked according to the highest category on a scale ranging from death (control, six; GR32191B, four) to nonfatal infarction (control, 22; GR32191B, 18), bypass grafting (control, 19; GR32191B, 22) and repeat angioplasty (control, 52; GR32191B, 48). No significant difference in ranking was detected. Six months after angioplasty, 75% of patients in the GR32191B group and 72% of patients in the control group were symptom free. CONCLUSIONS: Long-term thromboxane A2-receptor blockade with GR32191B does not prevent restenosis and does not favorably influence the clinical course after angioplasty.

Angioplasty, Balloon, Coronary↗
PubMed1990

Production of carrier-free 66Ga and labeling of antimyosin antibody for positron imaging of acute myocardial infarction.

A method for labeling monoclonal antimyosin antibodies with 66Ga is described. The radionuclide is a positron emitter (t1/2: 9.4h) produced by means of the 63Cu (4He, n) 66Ga reaction. Purification of the 66Ga from the copper target is described in detail. Monoclonal antimyosin antibodies are labeled with 66Ga at a high yield (99%) by transcomplexation from an acetate buffer with the diethylenetriamine pentaacetic acid (DTPA)-labeled antibody and preliminary evaluated in two dogs for imaging of myocardial necrosis by positron emission tomography.

Animals↗
PubMed1990

Wide-range load shift of combined aortic valvuloplasty-arterial vasodilation slows isovolumic relaxation of the hypertrophied left ventricle.

To assess the effects of left ventricular (LV) load on isovolumic relaxation rate of the hypertrophied LV, wide range LV load shifts were imposed by the sequential use of balloon aortic valvuloplasty (BAV) and arterial vasodilation in 14 patients with severe sclerocalcific aortic stenosis (aortic valve area, 0.45 +/- 0.16 cm2). Micromanometer tip-catheter LV pressure recordings (n = 14) and simultaneous LV angiograms (n = 9) were obtained before BAV, during nitroprusside infusion (NIT) before BAV, 48 hours after BAV, and 48 hours after BAV during NIT. LV peak systolic pressure (LVPSP) decreased from 237 +/- 33 mm Hg before BAV to 200 +/- 33 mm Hg (p less than 0.01) during NIT before BAV, to 201 +/- 27 mm Hg (p less than 0.01) after BAV and to 165 +/- 26 mm Hg (p less than 0.01) during NIT after BAV.LV end-systolic volume (LVESV) decreased from 55 +/- 34 ml before BAV to 25 +/- 23 ml (p less than 0.01) during NIT before BAV, to 30 +/- 32 ml (p less than 0.025) after BAV and to 15 +/- 12 ml (p less than 0.025) during NIT after BAV. LV end-systolic wall stress (LVESs) decreased from 90 +/- 30.10(3) dyne/cm2 before BAV to 41 +/- 13.10(3) dyne/cm2 (p less than 0.01) during NIT before BAV, to 55 +/- 16.10(3) dyne/cm2 (p less than 0.025) after BAV and to 26 +/- 6.10(3) dyne/cm2 (p less than 0.01) during NIT after BAV. Only after sequential BAV-NIT was the time of LV electromechanical systole (LVEST), which marked the onset of the LV isovolumic relaxation period, significantly reduced (from 419 +/- 26 msec before BAV to 363 +/- 28 msec after BAV-NIT [p less than 0.01]). The time constants of LV pressure decay with zero or nonzero asymptote pressure (TO and TPB) remained unchanged after BAV and during NIT before BAV. At the lowest LVPSP, LVESV, and LVESs after sequential BAV-NIT, both TO and TPB significantly prolonged from 35.7 +/- 6.3 to 46.7 +/- 12.6 msec (p less than 0.025) and from 46.6 +/- 12.5 to 73.2 +/- 23.3 msec (p less than 0.01). Phase-plane plots (LV dP/dt vs. LVP) of the LV pressure (P) signal during isovolumic relaxation were constructed for the four different loading states by matching corresponding LVP and LV dP/dt points. For a given LVP value, the corresponding LV dP/dt values on the phase plane plots were comparable before BAV, during NIT before BAV, and after BAV. The corresponding LV dP/dt value was higher during NIT after BAV, impling a slower relaxation rate at the same LVP after sequential BAV-NIT. A shift in the control of isovolumic LV relaxation kinetics from myofilamentary detachment to myoplasmic calcium removal, which proceeds slower in hypertrophied myocardium, could explain the observed slowing of LV isovolumic relaxation after drastic LV unloading of sequential BAV-NIT.

Aged↗
PubMed1990

[Alpha-adrenergic control of coronary circulation and left ventricular function during exertion].

Sympathetic activation is responsible for a striking inotropic and chronotropic response as well as for important coronary hyperemia during exercise. However the exact role of the coronary and myocardial alpha adrenergic receptors during sympathetic activation is not well defined. It is well accepted that coronary artery smooth muscle contains both alpha-1 and alpha-2 adrenergic receptors which elicit a vasoconstrictor response upon neurogenic and humoral stimulation. It seems however paradoxical that coronary vasoconstriction should occur in conditions of increased myocardial oxygen consumption such as during exercise. On the other hand, presynaptic alpha-2 receptors have been identified at the sympathetic nerve endings which, when stimulated by the locally released norepinephrine, will attenuate further norepinephrine release through a negative feed-back mechanism. A possible regulatory role of this mechanism for the left ventricular and coronary flow response during exercise has not been established. The major goal of this work was to define the exact role of alpha adrenergic receptors for the regulation of cardiac function and coronary circulation during exercise. Left ventricular function, coronary circulation, myocardial metabolism and catecholamine release were analysed during standardized treadmill exercise in conscious chronically instrumented dogs, prior to and following the administration of different alpha receptor blockers with different affinities for the different subtypes of alpha receptors. Three series of experiments were conducted to clarify: 1. the role of postsynaptic alpha receptors for the regulation of coronary blood flow during exercise, 2. the role of presynaptic alpha receptors for the regulation of left ventricular function during exercise, and 3. the role of postsynaptic alpha receptors for the regulation of transmural myocardial blood flow distribution during exercise. Dogs were instrumented with a solid state pressure transducer in the left ventricular cavity, a Doppler flow probe around the left circumflex coronary artery, and silastic catheters in aorta, left atrium and coronary sinus. 2-3 weeks after surgery the dogs were subjected to standard treadmill exercise. Simultaneous and continuous measurements were performed of heart rate, left ventricular systolic and end diastolic pressure, LV dP/dt/P, mean arterial pressure, late diastolic coronary vascular resistance, regional myocardial blood flow, myocardial oxygen consumption and plasma catecholamines. In the first series of experiments, coronary blood flow and myocardial oxygen consumption were analyzed in 15 conscious dogs at rest and during exercise prior to and following IV administration of phentolamine (1 mg/kg) or prazosin (0.5 mg/kg).(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1990

Effect of asynchrony on left ventricular relaxation.

The potential adverse effect of 1) electrical nonuniformity induced by right ventricular pacing and 2) mechanical nonuniformity observed in a model of stunned myocardium induced by 1 hour of severe coronary artery stenosis on left ventricular contraction and relaxation was studied in conscious dogs instrumented for long-term measurements of global and regional left ventricular function. Altering the sequence of electrical activation resulted in a significant change in contraction and relaxation predominantly through asynchrony rather than through changes in inotropy or loading conditions. In the presence of abnormal depolarization, sympathetic stimulation induced by treadmill exercise does not restore synchrony but, on the contrary, results in a significant prolongation of relaxation constant T1. During the early phase of reperfusion after 1 hour of severe coronary artery stenosis, left ventricular relaxation constant T1 is prolonged, whereas at the same time, temporal and regional asynchrony between the normal zone and the stunned zone are significantly augmented. The similarity between the time course of recovery of both global left ventricular relaxation and asynchrony suggests that asynchronous contraction, rather than regional relaxation abnormalities of the stunned myocardium, is the major cause for prolonged relaxation constant T1 during recovery from myocardial ischemia.

Animals↗
PubMed1988

Impaired relaxation of the hypertrophied left ventricle in aortic stenosis: effects of aortic valvuloplasty and of postextrasystolic potentiation.

Impaired left ventricular (LV) filling in aortic stenosis (AS) is explained by slow LV pressure decay, which impedes LV inflow. This slow LV pressure decay could be explained by the altered myocardial wall stress pattern of AS or by a failure of inactivation of hypertrophied myocardium. To evaluate whether altered LV loading or impaired myocardial inactivation is the predominant control of LV relaxation and filling in AS, we studied the effects of aortic valvuloplasty (PTAV) and of postextrasystolic potentiation (PESP). LV micromanometer tip pressure recordings and simultaneous LV angiograms were obtained before and after PTAV in 10 patients with AS. PTAV reduced peak-to-peak aortic valve gradient from 101 +/- 7 to 40 +/- 5 mmHg (P less than 0.01), peak LV systolic pressure from 211 +/- 8 to 169 +/- 4 mmHg (P less than 0.01) and LV end-diastolic pressure from 22 +/- 3 to 13 +/- 2 mmHg (P less than 0.01). Despite these large drops of LV loading after PTAV, the time constant, T, of LV pressure decay decreased only slightly from 47 +/- 4 to 44 +/- 4 ms (P less than 0.05) and the LV peak filling rate remained unaltered. The influence of PESP on LV relaxation and filling was investigated in patients with AS using LV micromanometer tip pressures (n = 22) and simultaneous mitral valve Doppler echocardiograms (n = 9). After PESP the time constant, T, of isovolumic LV pressure decay increased from 43 +/- 4 to 54 +/- 4 ms (P less than 0.01).2+ 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Aortic Valve↗
PubMed1988

Effects of asynchrony on myocardial relaxation at rest and during exercise in conscious dogs.

The effect of left ventricular asynchrony induced by right ventricular pacing on relaxation indexes was studied at rest and during exercise in seven conscious dogs instrumented for chronic measurements of left ventricular pressure, coronary blood flow, and arterial pressure and with right atrial and ventricular pacing electrodes. Increasing heart rate with atrial pacing resulted in an increase in both left ventricular maximum and minimum rates of pressure development, LV dP/dtmax and LV dP/dtmin, respectively, as well as in a decrease in the relaxation constant T. In contrast, increasing heart rate with ventricular pacing resulted in a decrease in LV dP/dtmax, a small increase in LV dP/dtmin, and a significant decrease in T. During exercise with heart rate kept constant with atrial pacing, both LV dP/dtmax and LV dP/dtmin increased and T decreased to the same extent as during exercise in sinus rhythm. In contrast, exercising during right ventricular pacing resulted in a significant increase in T, expressing a slowing of relaxation. It is concluded that increasing heart rate alone in the presence of asynchrony of LV contraction induced by abnormal electrical activation results in a depressed contractile response, while the relaxation phase is not significantly affected. However, during sympathetic stimulation, a condition where synchronization should be improved, the relaxation phase is considerably lengthened.

Adaptation, Physiological↗
PubMed1988

Late coronary spasm complicating successful angioplasty of the left main coronary artery.

A patient with successful percutaneous transluminal coronary angioplasty of the left main coronary artery is described. Two days later coronary angiography was performed because of recurrence of angina pectoris. Spontaneous spasm at the angioplasty site was documented. This potentially lethal complication issues a severe warning against angioplasty of the left main trunk.

Angiography↗
PubMed1988

Postextrasystolic potentiation worsens fast filling of the hypertrophied left ventricle in aortic stenosis and hypertrophic cardiomyopathy.

Impaired left ventricular (LV) filling in aortic stenosis (AS) and in hypertrophic cardiomyopathy (HCM) is caused by slow LV pressure decay, which could be explained by depressed inactivation of hypertrophied myocardium. Postextrasystolic potentiation (PESP), which increases activator calcium, could lead to further deterioration of LV relaxation. The influence of PESP on LV filling dynamics was, therefore, investigated in normal controls and in patients with LV hypertrophy caused by AS or by HCM. LV hemodynamics and LV hemodynamic relaxation indexes were determined during normal sinus rhythm (NSR) and after PESP. LV pressures were recorded by micromanometer tip catheters (controls, n = 10; AS, n = 17; HCM, n = 11). Simultaneous mitral flow Doppler echocardiograms were obtained in patients with LV hypertrophy (AS, n = 8, HCM, n = 5). Despite significant increases of LV dP/dtmax after PESP in all three study groups, PESP affected LV hemodynamic relaxation indexes differently. The time constant of LV pressure decay (TPB) derived from exponential curve fits with nonzero asymptote pressure remained unaltered after PESP in normal controls, rose from 62 +/- 17 to 74 +/- 21 msec (p less than 0.02) in patients with AS, and rose from 74 +/- 18 to 84 +/- 19 msec (p less than 0.02) in patients with HCM. Early diastolic LV pressure decay was measured by phi (phase of the first harmonic of a Fourier transform applied to the diastolic LV pressure waves) and by t (time interval from LV dP/dtmin to LV minimum diastolic pressure). After PESP, phi remained unaltered in normal controls but decreased in AS from 42.8 +/- 19.1 degrees to 24.0 +/- 28.8 degrees (p less than 0.001) and in HCM from 39.7 +/- 15.4 degrees to 26.9 +/- 15.7 degrees (p less than 0.001). Similarly, t was unchanged after PESP in normal controls but prolonged in AS from 146 +/- 48 to 205 +/- 86 msec (p less than 0.001) and in HCM from 168 +/- 40 to 208 +/- 53 msec (p less than 0.02).(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1986

Embolization complicating coronary angioplasty in the presence of an intracoronary thrombus.

Two cases of coronary occlusion and subsequent embolization during percutaneous coronary angioplasty (PTCA) are described. Prior to PTCA, angiographic evidence of intracoronary thrombus was present. Abrupt reclosure after dilation was treated by successful redilation. However, coronary embolization of thrombus debris occurred downstream in one patient and into an adjacent coronary branch in the second patient.

Angioplasty, Balloon↗