John W. Hirshfeld

Restenosis after coronary angioplasty: A multilvariate statistical model to relate lesion and procedure variables to restenosis☆

The Multi-Hospital Eastern Atlantic Restenosis Trial group obtained follow-up angiography in 510 patients with 598 successfully dilated coronary lesions who were enrolled in a controlled trial of the effects of a single dose of 1 g of methylprednisolone on restenosis after coronary angioplasty. The overall restenosis rate was 39.6%. The strongest univariate relations to the restenosis rate were found for lesion location (saphenous vein graft, 68%; left anterior descending artery, 45%; left circumflex artery and right coronary artery, 32%; p = 0.002); lesion length (≤4.6 mm, 33%; >4.6 mm, 45%; p = 0.001); percent stenosis before angioplasty (≤73%, 25%; >73%, 43%; p = 0.005), percent stenosis after angioplasty (≤21%, 33%; >21%, 46%; p = 0.017) and arterial diameter (<2.9 mm, 44%; ≥ 2.9 mm, 34%; p = 0.036). n nTwo multivariate models to predict restenosis probability were developed with use of stepwise logistic regression. The preprocedural model, which included only variables whose values were known before angioplasty, entered lesion length, vein graft location, left anterior descending artery location, percent stenosis before angioplasty, eccentric lesion and arterial diameter. The postprocedural model, which also included variables whose values were known after angioplasty was performed, was similar to the preangioplasty model except that it also entered postangioplasty percent stenosis and “optimal” balloon sizing but did not enter eccentric lesion. n nThese data indicate that the probability of restenosis after angioplasty is determined predominantly by the characteristics of the lesion being dilated. They are consistent with the known intimal proliferative mechanism of restenosis, offer a means of identifying lesions at unusually high or low risk of restenosis, and of predicting the likelihood that a particular lesion will restenose after angioplasty and provide a rationale for stratification by restenosis probability in the design of future studies of restenosis.

Three-year clinical follow-up after Palmaz-Schatz stenting

OBJECTIVESnOur goals were to examine late clinical outcome in a cohort of patients who electively received Palmaz-Schatz intracoronary stents, to identify specific predictors of outcome and to determine the time course of the development of ischemic cardiac events after stenting.nnnBACKGROUNDnShort-term results of Palmaz-Schatz intracoronary stenting have been promising, with a reduction in both angiographic restenosis and clinical cardiac events up to 1 year after stenting.nnnMETHODSnWe analyzed the clinical outcomes in 65 consecutive patients who underwent stenting at least 3 years before analysis. Demographic, clinical and procedural predictors of survival and event-free survival, defined as freedom from myocardial infarction, stent-site percutaneous transluminal coronary angioplasty, coronary artery bypass graft surgery or death, were analyzed at a mean follow-up of 39 +/- 17 months.nnnRESULTSnAbsolute survival and event-free survival at 3 years were 88% and 56%, respectively. Three-year freedom from stent-site revascularization was 66%. Predictors of decreased long-term survival (p < 0.05) included diabetes and a high angina score (Canadian Cardiovascular Society class III/IV) at 6 and 12 months after stenting. Predictors of decreased event-free survival (p < 0.05) included a high angina score at 3, 6 and 12 months after stenting, smaller stent deployment balloon size and greater number of stents implanted. Freedom from adverse events by 6 months after stenting also correlated with long-term event-free survival. Eighty-five percent of stent-site revascularizations occurred within 1 year. During late follow-up (>24 months), no patients had stent-site stenoses requiring revascularization, whereas 11% of patients required revascularization in nonstented coronary segments.nnnCONCLUSIONSnClinical predictors of worse long-term outcome included diabetes mellitus, higher angina score at follow-up, smaller stent deployment balloon size and greater number of stents at implantation. During follow-up, the majority of adverse events and stent-site revascularizations occurred early after stenting, and disease progression in nonstented vessels accounted for the majority of late revascularization events.

Intravascular ultrasonographic assessment of the results of coronary artery stenting

We studied 12 patients undergoing elective coronary stent implantation for either recurrent restenosis or adverse lesion appearance. By use of a 4.8F 20 MHz intravascular ultrasound catheter, the conventional angioplasty site was examined before and after coronary stent implantation. Quantitative angiographic analysis revealed the expected excellent final result with a group mean poststent diameter reduction of 14 +/- 9% and a cross-sectional area reduction of 22 +/- 13%. Angiographic analysis also indicated an increase in minimum stenosis diameter from 1.8 +/- 0.6 mm after conventional balloon angioplasty to 2.8 +/- 0.3 mm after coronary stent implantation. Quantitative analysis of the corresponding intravascular ultrasound images, however, revealed significant residual endoluminal obstruction. Fractional plaque area remained unchanged from 30 +/- 12% after conventional balloon angioplasty to 32 +/- 11% after stent implantation. The circumferential distribution of plaque increased significantly from 0.44 +/- 0.17 to 0.55 +/- 0.15 (p = 0.03) after stent implantation. Despite the lack of significant change in the ultrasound-determined minimum stenosis diameter after stent placement, there was a borderline significant increase in the plaque-free lumen area (before stent, 6.35 +/- 1.55 mm2; after stent, 7.25 +/- 1.6 mm2; p = 0.06). Thus, in contrast to the substantial improvement in the angiographically assessed residual luminal obstruction after stent implantation compared with the prestent condition, considerably less improvement was found by intravascular ultrasound-assessed examination. Morphometric analysis indicated a tendency toward circumferential remodeling of plaque. The inherently different approaches to vascular imaging represented by contrast angiography and intravascular ultrasound techniques appear to provide complementary information.(ABSTRACT TRUNCATED AT 250 WORDS)

Hemodynamic changes induced by cardiac angiography with ioxaglate: Comparison with diatrizoate

The hemodynamic and electrocardiographic changes induced by left ventriculography and coronary arteriography with ioxaglate (a new low osmolality angiographic contrast agent) were characterized and compared with the changes induced by a commercial formulation of the commonly used angiographic contrast agent, diatrizoate (Renografin-76). Left ventriculography and coronary arteriography were performed in 25 patients utilizing ioxaglate and in another 25 patients utilizing diatrizoate. Both agents increased left ventricular end-diastolic pressure and decreased arteriovenous oxygen difference after left ventriculography, but the magnitude of the increase caused by ioxaglate was significantly less than that caused by diatrizoate (changes in left ventricular end-diastolic pressure was 5.3 +/- 1.3 mm Hg with ioxaglate and 9.5 +/- 1.5 mm Hg with diatrizoate [p less than 0.02] ). Change in arteriovenous oxygen difference was -0.33 +/- 0.19 ml/100 ml with ioxaglate and -0.85 +/- 0.13 ml/100 ml with diatrizoate (p less than 0.05). Both agents were well tolerated when used for coronary arteriography with no adverse events occurring in either group. Ioxaglate is a well tolerated cardiac angiographic contrast agent that produces less hemodynamic disturbance than diatrizoate. Accordingly, it may be particularly well suited to use in patients with impaired left ventricular function.

Safety of cardiac angiography with conventional ionic contrast agents

To characterize the frequency of adverse reactions to conventional ionic contrast agents, data describing the frequency of such reactions were gathered from 4,630 diagnostic cardiac angiographic procedures. The patient population had a large prevalence of severe or unstable cardiac disease (56% had New York Heart Association class III, IV or V, 12.6% had left ventricular end-diastolic pressure greater than 25 mm Hg and 34% had 3-vessel or left main coronary artery disease). The overall minor adverse reaction rate was 14.2%. Major adverse reactions (requiring treatment) occurred in 61 (1.3%) of procedures. All adverse reactions were managed successfully and there were no deaths. Adverse reactions were more frequent in patients with higher New York Heart Association classes and with elevated left ventricular end-diastolic pressure. The adverse reaction rate was not increased in patients with more extensive coronary artery disease, reduced left ventricular ejection fraction or reduced cardiac index. The overall adverse reaction rate was probably influenced by physician behavior. Smaller volumes of contrast agent were administered to patients with more severe cardiac disease. Six percent of procedures were abbreviated either because of an adverse reaction or of concern that a reaction might occur if the procedure were continued. As a result, the diagnostic data obtained were judged to be inadequate in 0.8% of procedures. These data demonstrate that appropriate operator caution within the highly monitored environment of the cardiac catheterization laboratory allows cardiac angiography to be performed safely with conventional ionic contrast agents in most patients.(ABSTRACT TRUNCATED AT 250 WORDS)To characterize the frequency of adverse reactions to conventional ionic contrast agents, data describing the frequency of such reactions were gathered from 4,630 diagnostic cardiac angiographic procedures. The patient population had a large prevalence of severe or unstable cardiac disease (56% had New York Heart Association class III, IV or V, 12.6% had left ventricular end-diastolic pressure >25 mm Hg and 34% had 3-vessel or left main coronary artery disease). The overall minor adverse reaction rate was 14.2%. Major adverse reactions (requiring treatment) occurred in 61 (1.3%) of procedures. All adverse reactions were managed successfully and there were no deaths. Adverse reactions were more frequent in patients with higher New York Heart Association classes and with elevated left ventricular end-diastolic pressure. The adverse reaction rate was not increased in patients with more extensive coronary artery disease, reduced left ventricular ejection fraction or reduced cardiac index. The overall adverse reaction rate was probably influenced by physician behavior. Smaller volumes of contrast agent were administered to patients with more severe cardiac disease. Six percent of procedures were abbreviated either because of an adverse reaction or of concern that a reaction might occur if the procedure were continued. As a result, the diagnostic data obtained were judged to be inadequate in 0.8% of procedures. These data demonstrate that appropriate operator caution within the highly monitored environment of the cardiac catheterization laboratory allows cardiac angiography to be performed safely with conventional ionic contrast agents in most patients. Nonionic contrast agents may offer an advantage of providing greater safety and allowing a better study completion rate in patients who are severely ill and hemodynamically precarious.

Matching of myocardial oxygen consumption to mechanical load in human left ventricular hypertrophy and dysfunction.

The coupling of myocardial oxygen consumption (MVO2) with its determinants in left ventricular hypertrophy in human beings is poorly understood. Therefore, thermodilution-derived coronary blood flow, MVO2 and left ventricular wall stress, obtained from simultaneous left ventricular M-mode echogram and pressure, were compared in 32 patients with various degrees of left ventricular hypertrophy. Patients were studied at rest and after mechanical load alteration with nitroglycerin or phenylephrine. Decreases in MVO2 (-5.7 +/- 0.8 ml/min; p less than 0.001) and the time integral of meridional ejection stress or shortening load (-1,297 +/- 152 X 10(3) dynes X s/cm2; p less than 0.001) were observed after nitroglycerin administration while increases in MVO2 (+5.5 +/- 0.7 ml/min; p less than 0.001) and shortening load (+1,412 +/- 137 X 10(3) dynes X s/cm2; p less than 0.001) were noted after phenylephrine. An index relating the change in MVO2 to the corresponding change in shortening load (SL), % delta MVO2/% delta SL, was significantly different in patients without (Group 1) and with (Group 2) clinical left ventricular failure. Left ventricular mass was similar in both groups. The mean % delta MVO2/% delta SL with phenylephrine in Group 1 (79.6 +/- 9.6) was greater than the index for Group 2 (35.5 +/- 6.1; p less than 0.005). With nitroglycerin, Group 2 patients exhibited a greater reduction in % delta MVO2/% delta SL (110.5 +/- 17.8) than Group 1 (54.0 +/- 9.4; p less than 0.01). In conclusion, in patients with left ventricular hypertrophy and dysfunction there appears to be a state of diminished coronary flow response to load augmentation. However, load reduction in patients with clinical left ventricular failure results in a more balanced relation between oxygen uptake and ejection stress.

Effect of high dose aspirin on coronary hemodynamics during pacing-induced myocardial ischemia

The effects of aspirin on coronary hemodynamics and transcardiac concentrations of thromboxane B2 (the stable metabolite of thromboxane A2) were determined at rest and during pacing-induced myocardial ischemia in 11 patients with coronary disease. Control coronary sinus pacing increased both arterial thromboxane B2 (331 +/- 70 to 623 +/- 132 pg/ml, p less than 0.02) and coronary sinus thromboxane B2 (184 +/- 3 to 403 +/- 156 pg/ml, p less than 0.05), but positive transmyocardial gradients developed in only three patients. After 650 mg of oral aspirin, more than 90% inhibition of in vitro thromboxane B2 production was demonstrated and circulating thromboxane B2 was undetectable at rest and during pacing in all patients. Despite these changes in thromboxane B2 concentrations, coronary blood flow was unchanged by aspirin at rest (107 +/- 14 versus 112 +/- 13 ml/min, p = NS) and during pacing (189 +/- 29 versus 181 +/- 25 ml/min, p = NS). Myocardial lactate extraction was also unchanged at rest (24 +/- 7 versus 19 +/- 5%, p = NS) and during pacing (5 +/- 6 versus 9 +/- 5%, p = NS). No change occurred in the anginal threshold. Thus, aspirin does not have the vasoconstrictive properties that have been reported with another cyclo-oxygenase inhibitor, indomethacin. These findings also suggest that thromboxane A2 production does not play a major role in the pathogenesis of stress-induced ischemia. Nonetheless, intracoronary thromboxane A2 production in some patients may potentiate platelet activation and coronary thrombosis. Such patients may benefit from long-term aspirin therapy and can be treated with aspirin without risk of adverse coronary hemodynamic effects.

2018 ACC/HRS/NASCI/SCAI/SCCT Expert Consensus Document on Optimal Use of Ionizing Radiation in Cardiovascular Imaging: Best Practices for Safety and Effectiveness

WRITING COMMITTEE MEMBERS John W. Hirshfeld Jr., MD, FACC, FSCAI, Chair | Victor A. Ferrari, MD, FACC, Co-Chair | Frank M. Bengel, MD† | Lisa Bergersen, MD, MPH, FACC | Charles E. Chambers, MD, FACC, MSCAI‡ | Andrew J. Einstein, MD, PhD, FACC | Mark J. Eisenberg, MD, MPH, FACC | Mark A. Fogel, MD, FACC | Thomas C. Gerber, MD, FACC | David E. Haines, MD, FACC§ | Warren K. Laskey, MD, MPH, FACC, FSCAI | Marian C. Limacher, MD, FACC | Kenneth J. Nichols, PhD# | Daniel A. Pryma, MD | Gilbert L. Raff, MD, FACCk | Geoffrey D. Rubin, MD, MBA, FNASCI¶ | Donnette Smith** | Arthur E. Stillman, MD, PhD, FNASCI | Suma A. Thomas, MD, MBA, FACC | Thomas T. Tsai, MD, MSc, FACC | Louis K. Wagner, PhD | L. Samuel Wann, MD, MACC

792-5.Three Year Follow-up After Intracoronary Stent Implantation

To identify predictors of long-term success following intracoronary stenting, we analyzed clinical outcome in 65 consecutive patients who electively received Palmaz-Schatz stents at least 3 years prior to analysis. 83 stents were successfully inserted in 63 of 65 patients (97%), of whom 49 (75%) were men and 16 (25%) were women, with a mean age (±SD) of 59xa0±xa09 years, 18 patients (28%) were diabetic. 16 patients (24%) required more than one stent. Indications for stenting included restenosis following prior PTCA (52%) and lesion complexity (43%). 10 patients (15%) received stents in saphenous vein grafts. Demographic, clinical, and procedural predictors of survival and event-free survival at a mean follow-up of 39xa0±xa017 months were analyzed. Event-free survival was defined as survival without MI, CABG, PTCA at the stent site, or recurrent target vessel ischemia. Survival and event-free survival at 3 years were 86% and 54%, respectively. Predictors of decreased long term survival (pxa0lxa00.05) included diabetes, and a high angina score (Canadian Heart Class 3–4) at 6 and 12 months following stenting. Predictors of decreased event-free survival (pxa0lxa00.05) included smaller balloon size at implantation, greater number of stents at the primary lesion, and high angina score at each follow-up interval. Freedom from adverse events by 6 months following stenting correlated with long term success. 35 of 44 patients (80%) with event-free survival at 6 months remained event-free at follow-up. During follow-up, 17 patients (27%) developed symptomatic stent restenosis, requiring primarily early revascularization; 18 patients (28%) developed symptomatic stenoses in other vessels, requiring primarily late revascularization. We conclude that (1) long term survival after stenting is excellent; (2) the need for late revascularization is dictated primarily by disease progression in non-stented vessels; and (3) long-term success of stenting is predicted by freedom from adverse events at 6 months.