Relation between single tomographic intravascular ultrasound image parameters and intracoronary Doppler flow velocity in patients with intermediately severe coronary stenoses.

BACKGROUND: Intravascular ultrasound (IVUS) imaging parameters have been suggested as criteria to determine coronary lesion significance before intervention. However, there has not been a systematic examination of combined anatomic and physiologic data in the same patients with coronary artery disease. METHODS AND RESULTS: To examine the relation between coronary flow reserve and IVUS parameters, 41 patients with intermediately severe coronary artery stenoses had measurements of coronary flow velocity (0.014-inch Doppler flow wire), coronary flow velocity reserve (CVR) (hyperemic/basal mean flow), IVUS imaging (2.9F, Cardiovascular Imaging Systems, Inc.), and quantitative coronary angiography before intervention. Correlations between physiologic and anatomic parameters were performed by simple regression. Results were also examined by patient subgroups with CVR > 1.8 or < 1.8 to assess differences in IVUS parameters. The angiographic percent diameter stenosis was 52% +/- 17% (range 18% to 95%). Mean CVR was 1.88 +/- 0.56 (range 0.9 to 3.18). IVUS minimal luminal diameter (r = 0.312, p = 0.047) and angiographic percent stenosis (r = 3.05, p = 0.052) were weakly related to poststenotic CVR. Comparing patients with CVR < 1.8, IVUS reference segment area, IVUS lumen area, and angiographic percent diameter stenosis was higher (17.7 +/- 0.3 vs 12.9 +/- 4.4 mm2, p < 0.05; 6.20 +/- 3.76 vs 4.34 +/- 2.00 mm2, p < 0.05; and 60% +/- 14% vs 46% +/- 17%, p < 0.01, respectively) than in the group with CVR > 1.8. CONCLUSIONS: Despite a precise determination of cross-sectional vessel areas and absolute dimensions by IVUS, single tomographic measurements did not correlate well with coronary physiologic responses. These data suggest that the physiologic data may be complementary to anatomic quantitative IVUS, enhancing information for coronary interventional decision making.

Impaired coronary vasodilator responsiveness as a cause of lactate production during pacing-induced ischemia in patients with angina pectoris and normal coronary arteries.

Subgroups of patients with angina pectoris and normal coronary arteries are known to have pacing-induced lactate production and, therefore, myocardial ischemia. To examine the mechanism of this pacing-induced ischemia, the effect of incremental atrial pacing on coronary blood flow and metabolism was studied in 27 patients with angina and normal coronary arteries. Seventeen patients continued to exhibit normal lactate extraction even at heart rates up to 160 beats/min (Group 1), whereas in 10 patients (Group 2) lactate extraction changed to production at the highest pacing rate. Coronary blood flow increased in Group 1 patients by 18, 41 and 75%, respectively, as heart rate was increased by 20 beat/min increments from 100 to 160 beats/min. In contrast, coronary blood flow increased by only 8, 7 and 14%, at the three respective pacing rates in Group 2. Between the heart rates of 100 and 160 beats/min, coronary vascular resistance decreased 32% in Group 1 patients but was unchanged in Group 2 patients. There was no significant change in the ratio of myocardial O2 consumption/rate-pressure product in Group 1 patients, but this ratio decreased from 0.91 +/- 0.26 ml O2 X min-1 X (mm Hg X beats/min)-1 to 0.53 +/- 0.11 (p less than 0.05) in Group 2 patients as heart rate increased from baseline to 160 beats/min. Thus, patients with angina and normal coronary arteries who develop ischemia with pacing have a decreased coronary vasodilator response that interferes with their ability to increase myocardial oxygen supply to match the higher demand.

Platelet hyperactivity in acute myocardial infarction in man--effects of prostacyclin.

There is increasing evidence that platelets play an important role in the pathogenesis of acute ischemic heart disease. Therefore, an understanding of factors which impact on platelet performance is important. The present study was undertaken 1. to characterize during evolving myocardial infarction (MI) platelet activity in the peripheral circulation and across the ischemic/infarcting myocardial compartment, the locus of presumed platelet hyperactivity, and 2. to evaluate the effects of prostacyclin (PGI2), a most potent antiplatelet agent and vasodilator. A total of 59 patients with evolving MI were studied. 22 patients were instrumented with arterial and coronary sinus catheters and received intravenous infusion of PGI2, 13 +/- 4.5 ng/kg/min (mean +/- SD), for 90 minutes. In 15 of these patients, who had an anterior MI, transcardiac platelet function and response to PGI2 were studied. The results are as follows: Plasma levels of beta-thromboglobulin (beta-TG) and of thromboxane B2 (TxB2), in vivo measures of platelet activity, are elevated three and ten fold. 6-keto-prostaglandin F1 alpha, the stable end product of PGI2, is less than 10 pg/ml, reflecting a leftward shift of the TxB2/PGI2 ratio. Platelets, circulating during evolving MI ("ischemic platelets") are hyperaggregable in response to adenosine diphosphate and relatively resistent to PGI2, both in vivo and in vitro. Concentrations of platelet cyclic adenosine monophosphate and the cAMP response to PGI2 are diminished. The platelet hyper-reactivity is most intense early during infarct evolution and decreases with time. Transcardiac measurements indicate that thromboxane is produced across the ischemic/infarcting compartment in ten of 15 patients with anterior MI. The antiplatelet effect of PGI2 is greatly diminished. In summary, the data define an abnormal pattern of platelet behavior during evolving MI characterized by a pro-aggregatory environment, heightened platelet re-activity, both in the peripheral and coronary circulation, and relative resistance to PGI2. The clinical consequence of the data are that the infarct patient in the acute phase may benefit from platelet function suppression and requires significantly greater doses of prostacyclin than normal subjects. The data also suggest future directions for therapeutic manipulation of platelet hyper-reactivity in the setting of acute myocardial ischemia.

Systemic and transcardiac platelet activity in acute myocardial infarction in man: resistance to prostacyclin.

There is increasing evidence that platelets play an important role in the pathogenesis of acute ischemic heart disease. Therefore an understanding of factors that influence platelet performance is important. This study was undertaken (1) to characterize during evolving myocardial infarction platelet activity in the peripheral circulation and across the ischemic/infarcting myocardial compartment, the locus of presumed platelet hyperactivity, and (2) to evaluate the effects of prostacyclin (PGI2), a most potent antiplatelet agent and vasodilator. A total of 59 patients with evolving myocardial infarction were studied. Twenty-two patients were instrumented with arterial and coronary sinus catheters and received intravenous infusion of PGI2, 13 +/- 4.5 ng/kg/min (mean +/- SD), for 90 min. In 15 patients with anterior myocardial infarction, transcardiac platelet function and response to PGI2 were studied. Plasma levels of beta-thromboglobulin (beta-TG) and of thromboxane B2 (TxB2), in vivo measures of platelet activity, were elevated three- and 10-fold. 6-Keto-prostaglandin F 1 alpha, the stable end product of PGI2, was less than 10 pg/ml, reflecting a leftward shift of the TxB2/PGI2 ratio. Platelets circulating during evolving myocardial infarction ("ischemic platelets") were hyperaggregable in response to ADP and relatively resistant to PGI2, both in vivo and in vitro. Concentrations of platelet cyclic AMP and the cyclic AMP response to PGI2 were diminished. The platelet hyperreactivity, expressed by plasma beta-TG, platelet aggregation, and PGI2-induced inhibition of aggregation, was most intense early during infarct evolution and decreased with time. The increased platelet performance resulted in "platelet fatigue," indicated by decreased contents of beta-TG of the ischemic platelet and decreased TxA2 production in response to collagen. However, the ischemic platelet produced twice normal TxA2 in response to arachidonic acid (stimulus and substrate), demonstrating a heightened metabolic capacity. TxA2 was produced across the ischemic/infarcting compartment in 10 of 15 patients with anterior myocardial infarction. The antiplatelet effect of PGI2 was greatly diminished. In summary, the data define an abnormal pattern of platelet behavior during evolving myocardial infarction, characterized by a proaggregatory environment, heightened platelet reactivity in both the peripheral and coronary circulation, and relative resistance to PGI2. The clinical consequences of the data are that the patient in the acute phase of myocardial infarction may benefit from suppression of platelet function and requires significantly greater doses of PGI2 than normal subjects.(ABSTRACT TRUNCATED AT 400 WORDS)

AAP periodicity guidelines: a framework for educating patients.

In 1967 the American Academy of Pediatrics published standards for periodic health supervision visits. In 1972 and 1975, in response to changes in child health needs, the guidelines were revised. The current AAP periodicity guidelines, adopted in 1981, provide for reasonable care and meet the minimum requirements for preventive health services for normal infants, children, and adolescents. Whereas detecting physical defects, evaluating illness, and assessing the child's development are key elements of the periodic visit, parent education is equally important. The educational aspects of a health supervision visit--which consists of interval history, measurements, sensory screening, developmental and behavioral assessment, physical examination, procedures, and anticipatory guidance--are stressed. A prenatal visit is important, particularly for first-time parents. Periodic visits are also valuable for adolescents, who face special concerns such as substance abuse, risk-taking behavior, and problems of sexuality. Often, the pediatrician may be the only professional whose advice and counsel the teenager will accept.

Results of endomyocardial biopsy in patients with spontaneous ventricular tachycardia but without apparent structural heart disease.

To evaluate possible occult myocardial disease in 18 patients whose only major manifestation of heart disease was spontaneous ventricular tachycardia or fibrillation, right ventricular endomyocardial biopsies were performed. None of the patients had symptoms of ischemic or congestive heart disease, and at catheterization none had significant lesions of the coronary arteries or regional wall motion abnormalities of the left ventricle. The mean left ventricular ejection fraction (65 +/- 7%), mean right ventricular ejection fraction (55 +/- 9%), mean cardiac index (3.0 +/- 0.5 1/min/m2), mean right atrial pressure, mean pulmonary capillary wedge pressure, and mean pulmonary artery systolic pressure were normal. However, right ventricular endomyocardial biopsy specimens were abnormal in 16 of 18 (89%) patients: nine (50%) had changes of a significant, although nonspecific, cardiomyopathy with myocellular hypertrophy, interstitial and perivascular fibrosis, and vascular sclerosis; three (17%) had subacute inflammatory myocarditis; two (11%) had diffuse abnormalities of the intramyocardial arteries; and two (11%) had pathologic changes consistent with arrhythmogenic right ventricular dysplasia. In the two (11%) patients with normal biopsy specimens, one had Wolff-Parkinson-White syndrome and the other had mitral valve prolapse. Although histologic abnormalities were found in 89% of these patients, performance of right ventricular endomyocardial biopsies in this group of patients should be considered a research procedure. We conclude that the majority of patients who have serious ventricular arrhythmias but no apparent structural cardiac abnormalities have abnormal right ventricular biopsy specimens and that the arrhythmias may be the first manifestation of a variety of primary myocardial abnormalities.