4
the primary predictor of survival after AMI, 9 this result supports the previous observation that elevated neutrophil counts on admission are associated with adverse outcome in AMI. It is an important issue to determine whether a larger extent of ischemic myocardial injury or infarc- tion at the time of admission causes elevated neutro- phil counts, or whether elevated neutrophil counts on admission cause a larger extent of myocardial damage after reperfusion therapy. In the present study, neutro- phil counts on admission tended to correlate with the sums of ST-segment elevation. This observation sug- gests that a larger extent of myocardial ischemic in- jury or infarction before reperfusion therapy is at least partially related to elevated neutrophil counts. Fur- thermore, the positive correlation between neutrophil counts on admission and time elapsed from the onset to admission suggests that the development of myo- cardial ischemic injury or infarction may lead to a time-dependent elevation in neutrophil counts in the early phase of AMI. However, we cannot deny the possibility that the higher neutrophil count on admis- sion is the cause of further myocardial damage after reperfusion. Experimental studies have indicated that neutrophil infiltration of the infarct territory is shown within 3 to 6 hours of coronary occlusion and is particularly pronounced after reperfusion. 10,11 Acti- vated neutrophils can cause reperfusion injury by hypercoagulation, 12 no-reflow, 13 and cardiotoxicity through oxygen-derived free radicals 14 and proinflam- matory cytokines such as tumor necrosis factor-a. 15 Thus, in our selected patients with anterior wall AMI, neutrophil counts on admission were associ- ated with infarct size evaluated by the peak crea- tine phosphokinase level, and with LV systolic function in the chronic phase. Our results support the previous observation that elevated neutrophil counts on admission are associated with adverse outcome in AMI. 1. Burr ML, Holliday RM, Fehily AM, Whitehead PJ. Haematological prognostic indices after myocardial infarction: evidence from the diet and reinfarction trial (DART). Eur Heart J 1992;13:166–170. 2. Furman MI, Becker RC, Yarzebski J, Savegeau J, Gore JM, Goldberg RJ. Effect of elevated leukocyte count on in-hospital mortality following acute myocardial infarction. Am J Cardiol 1996;78:945–948. 3. Barron HV, Cannon CP, Murphy SA, Braunwald E, Gibson CM. Association between white blood cell count, epicardial blood flow, myocardial perfusion, and clinical outcomes in the setting of acute myocardial infarction: a Thrombolysis In Myocardial Infarction 10 substudy. Circulation 2000;102:2329–2334. 4. Kyne L, Hausdorff JM, Knight E, Dukas L, Azhar G, Wei JY. Neutrophilia and congestive heart failure after acute myocardial infarction. Am Heart J 2000;139: 94–100. 5. The TIMI Study Group. The Thrombolysis In Myocardial Infarction (TIMI) trial. N Engl J Med 1985;312:932–936. 6. Rentrop KP, Cohen M, Blanke H, Phillips RA. Changes in collateral channel filling immediately after controlled coronary artery occlusion by an angioplasty balloon in human subjects. J Am Coll Cardiol 1985;5:587–592. 7. Kennedy JW, Trenholme SE, Kasser IS. Left ventricular volume and mass from single-plane cineangiocardiograms: a comparison of antero-posterior and right anterior oblique methods. Am Heart J 1970;80:343–352. 8. Sheehan FH, Bolson EL, Dodge HT, Mathey DG, Schofer J, Woo HW. Advantages and applications of the centerline method for characterizing regional ventricular function. Circulation 1986;74:293–305. 9. White HD, Norris RM, Brown MA, Brandt PWT, Whitlock RML, Wild CJ. Left ventricular end-systolic volume as the major determinant of survival after recovery from myocardial infarction. Circulation 1987;76:44–51. 10. Engler RL, Dahlgren MD, Peterson MA, Dobbs A, Schmid-Schoenbein GW. Accumulation of polymorphonuclear leukocytes during 3 hour experimental myocardial ischemia. Am J Physiol 1986;251:H93–H100. 11. Mehta JL, Nochols WW, Mehta P. Neutrophils as potential participants in acute myocardial ischemia: relevance to reperfusion. J Am Coll Cardiol 1988; 11:1309–1316. 12. Ott I, Neumann FJ, Kenngott S, Gawaz M, Schomig A. Procoagulant inflammatory responses of monocytes after direct balloon angioplasty in acute myocardial infarction. Am J Cardiol 1998;82:938–942. 13. Engler RL, Schmid-Schonbein GW, Pavelec RS. Leukocyte capillary plug- ging in myocardial ischemia and reperfusion in the dog. Am J Pathol 1983;111: 98–111. 14. McCord JM. Oxygen-derived free radicals in postischemic tissue injury. N Engl J Med 1985;312:159–163. 15. Mann DL, Young JB. Basic mechanisms in congestive heart failure: recog- nizing the role of proinflammatory cytokines. Chest 1994;105:897–904. Primary Angioplasty for Acute Myocardial Infarction in Octogenarians Shlomi Matetzky, MD, Tali Sharir, MD, Marko Noc, MD, Michelle Domingo, BSc, Kuang-Yuh Chyu, MD, Saibal Kar, MD, Neal Eigler, MD, Sanjay Kaul, MD, Prediman K. Shah, MD, and Bojan Cercek, MD I n patients with acute myocardial infarction (AMI), mortality increases sharply in the elderly and reaches .30% in octogenarian patients. 1–3 El- derly patients are less likely to receive thrombolytic therapy 4–8 and the risk of hemorrhagic complica- tions is higher. 9–15 Although primary percutaneous coronary interventions (PCI) with angioplasty and stenting may offer an attractive alternative for these patients, only few and conflicting data exist regard- ing the effect of advanced age on success rate, complications, and clinical outcome of primary PCI. In the present study, we report angiographic and clinical outcomes and complications of primary PCI in 48 consecutive octogenarians, and compare these results with those of younger patients in the same series of patients. From the Division of Cardiology, Cedars-Sinai Medical Center/UCLA School of Medicine, Los Angeles, California. Drs. Matetzky and Sharir were supported by the Save A Heart Foundation, Los Angeles, Cali- fornia; and Dr. Noc was supported by the Slovenian Science Foun- dation and University Medical Center, Ljubljana, Slovenia. Dr. Cer- cek’s address is: Division of Cardiology, Cedars-Sinai Medical Cen- ter, Room 5314, 8700 Beverly Boulevard, Los Angeles, California 90048-1865. E-mail: [email protected]. Manuscript received March 20, 2001; revised manuscript received and accepted May 11, 2001. 680 ©2001 by Excerpta Medica, Inc. All rights reserved. 0002-9149/01/$–see front matter The American Journal of Cardiology Vol. 88 September 15, 2001 PII S0002-9149(01)01816-1

Primary angioplasty for acute myocardial infarction in octogenarians

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Page 1: Primary angioplasty for acute myocardial infarction in octogenarians

the primary predictor of survival after AMI,9 thisresult supports the previous observation that elevatedneutrophil counts on admission are associated withadverse outcome in AMI.

It is an important issue to determine whether alarger extent of ischemic myocardial injury or infarc-tion at the time of admission causes elevated neutro-phil counts, or whether elevated neutrophil counts onadmission cause a larger extent of myocardial damageafter reperfusion therapy. In the present study, neutro-phil counts on admission tended to correlate with thesums of ST-segment elevation. This observation sug-gests that a larger extent of myocardial ischemic in-jury or infarction before reperfusion therapy is at leastpartially related to elevated neutrophil counts. Fur-thermore, the positive correlation between neutrophilcounts on admission and time elapsed from the onsetto admission suggests that the development of myo-cardial ischemic injury or infarction may lead to atime-dependent elevation in neutrophil counts in theearly phase of AMI. However, we cannot deny thepossibility that the higher neutrophil count on admis-sion is the cause of further myocardial damage afterreperfusion. Experimental studies have indicated thatneutrophil infiltration of the infarct territory is shownwithin 3 to 6 hours of coronary occlusion and isparticularly pronounced after reperfusion.10,11 Acti-vated neutrophils can cause reperfusion injury byhypercoagulation,12 no-reflow,13 and cardiotoxicitythrough oxygen-derived free radicals14 and proinflam-matory cytokines such as tumor necrosis factor-a.15

Thus, in our selected patients with anterior wallAMI, neutrophil counts on admission were associ-ated with infarct size evaluated by the peak crea-tine phosphokinase level, and with LV systolicfunction in the chronic phase. Our results support

the previous observation that elevated neutrophilcounts on admission are associated with adverseoutcome in AMI.

1. Burr ML, Holliday RM, Fehily AM, Whitehead PJ. Haematological prognosticindices after myocardial infarction: evidence from the diet and reinfarction trial(DART). Eur Heart J1992;13:166–170.2. Furman MI, Becker RC, Yarzebski J, Savegeau J, Gore JM, Goldberg RJ.Effect of elevated leukocyte count on in-hospital mortality following acutemyocardial infarction.Am J Cardiol1996;78:945–948.3. Barron HV, Cannon CP, Murphy SA, Braunwald E, Gibson CM. Associationbetween white blood cell count, epicardial blood flow, myocardial perfusion, andclinical outcomes in the setting of acute myocardial infarction: a Thrombolysis InMyocardial Infarction 10 substudy.Circulation 2000;102:2329–2334.4. Kyne L, Hausdorff JM, Knight E, Dukas L, Azhar G, Wei JY. Neutrophilia andcongestive heart failure after acute myocardial infarction.Am Heart J2000;139:94–100.5. The TIMI Study Group. The Thrombolysis In Myocardial Infarction (TIMI)trial. N Engl J Med1985;312:932–936.6. Rentrop KP, Cohen M, Blanke H, Phillips RA. Changes in collateral channelfilling immediately after controlled coronary artery occlusion by an angioplastyballoon in human subjects.J Am Coll Cardiol1985;5:587–592.7. Kennedy JW, Trenholme SE, Kasser IS. Left ventricular volume and massfrom single-plane cineangiocardiograms: a comparison of antero-posterior andright anterior oblique methods.Am Heart J1970;80:343–352.8. Sheehan FH, Bolson EL, Dodge HT, Mathey DG, Schofer J, Woo HW.Advantages and applications of the centerline method for characterizing regionalventricular function.Circulation 1986;74:293–305.9. White HD, Norris RM, Brown MA, Brandt PWT, Whitlock RML, Wild CJ.Left ventricular end-systolic volume as the major determinant of survival afterrecovery from myocardial infarction.Circulation 1987;76:44–51.10. Engler RL, Dahlgren MD, Peterson MA, Dobbs A, Schmid-Schoenbein GW.Accumulation of polymorphonuclear leukocytes during 3 hour experimentalmyocardial ischemia.Am J Physiol1986;251:H93–H100.11. Mehta JL, Nochols WW, Mehta P. Neutrophils as potential participants inacute myocardial ischemia: relevance to reperfusion.J Am Coll Cardiol1988;11:1309–1316.12. Ott I, Neumann FJ, Kenngott S, Gawaz M, Schomig A. Procoagulantinflammatory responses of monocytes after direct balloon angioplasty in acutemyocardial infarction.Am J Cardiol1998;82:938–942.13. Engler RL, Schmid-Schonbein GW, Pavelec RS. Leukocyte capillary plug-ging in myocardial ischemia and reperfusion in the dog.Am J Pathol1983;111:98–111.14. McCord JM. Oxygen-derived free radicals in postischemic tissue injury.N Engl J Med1985;312:159–163.15. Mann DL, Young JB. Basic mechanisms in congestive heart failure: recog-nizing the role of proinflammatory cytokines.Chest1994;105:897–904.

Primary Angioplasty for Acute Myocardial Infarctionin Octogenarians

Shlomi Matetzky, MD, Tali Sharir, MD, Marko Noc, MD, Michelle Domingo, BSc,Kuang-Yuh Chyu, MD, Saibal Kar, MD, Neal Eigler, MD, Sanjay Kaul, MD,

Prediman K. Shah, MD, and Bojan Cercek, MD

In patients with acute myocardial infarction(AMI), mortality increases sharply in the elderly

and reaches.30% in octogenarian patients.1–3 El-

derly patients are less likely to receive thrombolytictherapy4 – 8 and the risk of hemorrhagic complica-tions is higher.9 –15 Although primary percutaneouscoronary interventions (PCI) with angioplasty andstenting may offer an attractive alternative for thesepatients, only few and conflicting data exist regard-ing the effect of advanced age on success rate,complications, and clinical outcome of primaryPCI. In the present study, we report angiographicand clinical outcomes and complications of primaryPCI in 48 consecutive octogenarians, and comparethese results with those of younger patients in thesame series of patients.

From the Division of Cardiology, Cedars-Sinai Medical Center/UCLASchool of Medicine, Los Angeles, California. Drs. Matetzky and Sharirwere supported by the Save A Heart Foundation, Los Angeles, Cali-fornia; and Dr. Noc was supported by the Slovenian Science Foun-dation and University Medical Center, Ljubljana, Slovenia. Dr. Cer-cek’s address is: Division of Cardiology, Cedars-Sinai Medical Cen-ter, Room 5314, 8700 Beverly Boulevard, Los Angeles, California90048-1865. E-mail: [email protected]. Manuscript received March20, 2001; revised manuscript received and accepted May 11,2001.

680 ©2001 by Excerpta Medica, Inc. All rights reserved. 0002-9149/01/$–see front matterThe American Journal of Cardiology Vol. 88 September 15, 2001 PII S0002-9149(01)01816-1

Page 2: Primary angioplasty for acute myocardial infarction in octogenarians

• • •The study comprised 181 consecutive patients with

AMI who underwent primary PCI for AMI with ST-segment elevation at Cedars-Sinai Medical Center fromJanuary 1997 to January 1999. During this period, pri-mary PCI was the standard therapy for patients present-ing within 12 hours of symptoms of an ST elevationAMI. Stent deployment and adjunctive therapy withIIb/IIIa inhibitors and intraaortic balloon pump wereused at the discretion of the attending physician. Allpatients received aspirin and clopidogrel or ticlopidin for4 weeks after stent deployment.

Coronary angiograms were interpreted by 2 investi-gators who were blinded to Thrombolysis In MyocardialInfarction (TIMI) trial flow grade in the infarct-relatedartery and a number of coronary arteries with significant($70%) stenosis. Successful PCI was defined as TIMI 3flow and a residual stenosis of,30%.

During hospital stay, patients were followed for theoccurrence of congestive heart failure (CHF), shock,and/or death. Major bleeding was defined as intracranialbleeding, bleeding with hemodynamic compromise, orbleeding requiring transfusion. Acute worsening of renalfunction was defined as any elevation in creatinine of.1.5 mg/dl, or with preexisting renal insufficiency, anincrease in creatinine level of$0.5 mg/dl.

Before discharge, left ventricular ejection fractionwas determined by 2-dimensional echocardiography. Af-ter discharge, patients were followed for an average of 18months (follow-up was completed by July 1999). Fol-low-up data were analyzed for total and cardiac mortal-ity, cardiac events (cardiac mortality and nonfatal rein-farction), and target vessel revascularization.

Comparison between groups was performed usingthet test for continuous variables and the chi-square orFisher’s exact test for categorical variables. Stepwisemultivariate logistic regression analysis was applied toidentify independent predictors of the prespecified endpoint of death, CHF, and shock during hospital stay.Stepwise multivariate hazard Cox regression was used

to identify the independent predic-tors of the occurrence of a cardiacevent during the follow-up period.

Of 181 consecutive patients in-cluded in the present study, 48 (27%)were aged$80 years (mean 846 5,range 80 to 94) and 133 patients(73%) were aged,80 years (mean60 6 11, range 28 to 77). Admissiondemographic and clinical character-istics are listed in Table 1.

Initial angiographic characteris-tics were similar in patients aged$80 and,80 years (Table 2). Afterdiagnostic angiography, 1 patientaged $80 years and 2 aged,80years were referred for urgent bypasssurgery because of extensive coro-nary artery disease. All other patientsunderwent primary PCI. PCI wassuccessful in 87% of both groups of

patients. Failure was due to inability to cross theculprit lesion in 8.5% and 4% of patients, and TIMIflow #2, despite adequate dilatation of the culpritlesion, was achieved in 4.5% and 9% of patients aged$80 and,80 years, respectively (p5 0.25). Therewere no significant differences in the use of temporarypacemaker (17% vs 10%, p5 0.21), intraaortic bal-loon pump (13% vs 8%, p5 0.4), or IIb/IIIa inhibitors(71% vs 83%, p5 0.11) in patients$80 and,80years of age, respectively.

Compared with younger patients, octogenarianshad a significantly higher incidence of CHF and atrend toward a higher incidence of cardiogenic shockand mortality (Table 3). Patients with versus thosewithout CHF had a higher incidence of PCI failure(32% vs 9%, p5 0.004). The combined end point ofCHF, cardiogenic shock, and/or mortality was signif-icantly more prevalent in octogenarians than inyounger patients (35% vs 17% p5 0.006). In multi-variate analysis, after adjustment for initial demo-graphic and clinical characteristics, use of intraaorticballoon pump (odds ratio [OR] 23, 95% confidenceinterval [CI] 4.8 to 117), Killip class (OR 6.2, 95% CI3 to 13), and success of primary PCI (OR 0.12, 95%CI 0.035 to 0.46) were the only independent predictorsof the combined end point. When any age and age$80 years were forced into this model they had nosignificant incremental value.

Intracranial hemorrhage or ischemic stroke did notoccur in either group. Octogenarians had a higherincidence of major bleeding (6.3% vs 1.5%, p50.12), minor bleeding (8.7% vs 5.3%, p5 0.18), andthrombocytopenia (4% vs 0.75%, p5 0.17), althoughnone was fatal. Patients aged$80 years had an in-creased risk of worsening of renal function (21% vs2.3%, p,0.001). Impaired renal function was presentbefore PCI in 8 of the 10 patients who developedworsening of renal function. No patient required he-modialysis and renal function improved at least par-tially in all.

A comparable proportion of octogenarians and

TABLE 1 Baseline Characteristics

Age (yrs)

p Value$80 (n 5 48) ,80 (n 5 133)

Men 27 (56%) 90 (68%) 0.16Previous myocardial infarct 23 (47%) 27 (20%) 0.002Congestive heart failure 4 (8.3%) 2 (1.5%) 0.043Coronary artery bypass graft surgery 6 (13%) 6 (4.5%) 0.085Family history of heart disease 9 (19%) 3 (25%) 0.4Hyperlipidemia 9 (19%) 70 (53%) 0.000Systemic hypertension 24 (50%) 7 (56%) 0.45Smoking 4 (8.3%) 37 (28%) 0.006Diabetes mellitus 6 (13%) 3 (28%) 0.053Time to presentation (min) (mean 6 SD) 237 6 250 190 6 196 0.3Leads with ST elevation 3.5 6 2.1 3.3 6 2.7 0.7Anterior wall infarction AMI 28 (58%) 66 (50%) 0.34Right ventricular infarction 4 (8.3%) 7 (5.3%) 0.45Killip class

Class I 27 (56%) 111 (83.5%)Class II 11 (23%) 12 (9%) 0.007Class III/IV 10 (21%) 10 (7.5%)

BRIEF REPORTS 681

Page 3: Primary angioplasty for acute myocardial infarction in octogenarians

younger patients had a Q-wave AMI pattern on thedischarge electrocardiogram (51% vs 54%, p5 0.79),and there was no significant difference in the predis-charge left ventricular ejection fraction (456 12% vs49 6 11%, p5 0.11).

Complete data were obtained for 42 of the octoge-narian survivors (95%) and for 117 of the survivors,80 years of age (91%) (Table 4). Postdischargeoctogenarians were followed for 18.26 8.8 comparedwith 18.46 8.0 months in younger patients (p5 0.9).As expected, octogenarians had a higher postdis-charge total mortality (17% vs 3.4%, p5 0.0065).Cardiac mortality was relatively low in both groups ofpatients, although insignificantly higher in octogenar-ians than in younger patients (7.1% and 1.7%, respec-tively; p 5 0.12). Of the 5 cardiac deaths 2, were due

to reinfarction, 1 occurred during by-pass surgery, and 2 deaths were sud-den. One patient each died of mes-enteric ischemia, stroke, and pulmo-nary embolism. Noncardiovasculardeaths were due to cancer in 2 andsepsis in 1 patient. There were nosignificant differences in the inci-dence of reinfarction, cardiac events,incidences of readmissions for an-gina or CHF, or need for bypass sur-gery during the 18-month follow-upperiod between the 2 groups. In uni-variate (Cox regression) analysis,failed primary PCI (p5 0.014) andCHF during hospitalization (p50.047) were the only significant pre-dictors of future cardiac events, andin multivariate analysis, both re-mained independent predictors ofoutcome.

• • •In this study we demonstrated

that primary PCI for ST elevationAMI in octogenarians has a successrate that is similar to younger pa-tients. The strategy applied in thisstudy of primary PCI, provisionalstenting, and the use of IIb/IIIa in-hibitors was safe and not associatedwith an increase in the risk of strokeor intracranial bleed. Octogenarianshad only a small increase in the riskof bleeding complications andthrombocytopenia, and had a signif-icantly higher risk of reversibleworsening of renal function thanyounger patients. The higher risk forcombined CHF, shock, or mortalityin octogenarians was not due to age,but to worse hemodynamic charac-teristics at admission, which are of-ten seen in the elderly.

Although thrombolytic therapyresults in a reperfusion rate in thevery elderly that is similar to that

in younger patients,7,16 mortality remains unfavor-ably high:$30% in patients aged.80 years.5,6,10,17

A recent large observational study even suggests thatthrombolytic therapy might be deleterious in patientsaged.75 years.18 In the present study we demon-strated a high success rate of primary PCI that wasassociated with relatively low in-hospital mortality of8% in ST elevation AMI patients aged$80 years. Thelow incidence of significant bleeding and strokestrengthened the apparent benefit of early reperfusionin elderly patients when compared with previous stud-ies of thrombolytic therapy.12–14

In the Global Use of Strategies To open Occludedcoronary arteries II (GUSTO IIB) study, the 30-daymortality among the 45 patients$80 years of agetreated with primary PCI was comparable to that of

TABLE 2 Angiographic Characteristics and Primary PCI Results

Ages (yrs)

p Value.80

(n 5 48),80

(n 5 133)

Infarct-related arteryLeft anterior descending 23 (48%) 57 (43%)Left circumflex 8 (17%) 22 (16.5%) 0.6Right 15 (31%) 54 (41.5%)Saphenous vein graft 2 (4%) 0 (0%)

Multivessel coronary disease 35 (73%) 88 (66%) 0.25TIMI flow $2 on initial angiogram 17 (35%) 38 (29%) 0.5Primary PCI success 41 (87%) 114 (87%) 1.0Stent deployment 25 (53%) 76 (58%) 0.6

TABLE 3 In-Hospital Clinical Course

Ages (yrs)

p Value.80

(n 5 48),80

(n 5 133)

Congestive heart failure 13 (27%) 17 (13%) 0.024Cardiogenic shock 6 (13%) 9 (6.8%) 0.23Recurrent angina 3 (6.3%) 11 (8.3%) 0.76Reinfarction 1 (2.1%) 2 (1.5%) 1.0Coronary artery bypass graft surgery (nonurgent) 2 (4.2%) 8 (6%) 1.0Ventricular tachycardia/ventricular

fibrillation6 (13%) 19 (14%) 0.86

Asystole 2 (4.2%) 3 (2.2%) 0.6Atrial fibrillation 5 (10%) 3 (2.2%) 0.032Left ventricular thrombus 1 (2.1%) 4 (3.0%) 1.0Death 4 (8.3%) 4 (3.0%) 0.21

TABLE 4 Long-Term Outcome (during postdischarge period)

Age (yrs)

p Value.80 (n 5 42) ,80 (n 5 117)

Reinfarction 3 (7.1%) 7 (6.0%) 0.71Readmission for angina 6 (14%) 29 (25%) 0.23Readmission for congestive heart failure 2 (4.8%) 3 (2.6%) 0.61Coronary artery bypass graft surgery 3 (7.1%) 14 (12%) 0.56Target-vessel revascularization 2 (4.8%) 22 (19%) 0.04Cardiac death 3 (7.1%) 2 (1.7%) 0.12Cardiac event* 5 (12%) 9 (7.7%) 0.74Total mortality 7 (17%) 4 (3.4%) 0.0065

*Cardiac event indicates cardiac mortality or nonfatal reinfarction.

682 THE AMERICAN JOURNAL OF CARDIOLOGYT VOL. 88 SEPTEMBER 15, 2001

Page 4: Primary angioplasty for acute myocardial infarction in octogenarians

patients treated with tissue plasminogen activator(26.7% and 27%, respectively).10 This was substan-tially higher than the 17% seen in our experience. Theless favorable outcome in the GUSTO study might bein part due to the lesser use of stents (5%) than used in.50% of our patients and the use of potent antiplatelettherapy instead of anticoagulation in our study. Theshift from anticoagulation to aggressive antiplatelettherapy appears to be especially beneficial in elderlypatients because of lower bleeding complications,stroke, and reinfarction.19 The early use of aggressiveantiplatelet therapy may also explain a relatively highincidence of TIMI flow.2 on the initial angiogram.Also, our study represents experience of a single cen-ter with a high volume of PCIs.

In contrast to a previous report,20 in our study therate of recurrent angina and the target vessel revascu-larization rate did not differ significantly betweenoctogenarians and younger patients.

We conclude that in octogenarians with ST eleva-tion AMI, primary angioplasty is safe and as effectivein achieving reperfusion as in younger patients.

1. Weaver WD, Litwin PE, Martin JS, Kudenchuk PJ, Maynard C, Eisenberg MS, HoMT, Cobb LA, Kennedy JW, Wirkus MS. Effect of age on use of thrombolytictherapy and mortality in acute myocardial infarction.J Am Coll Cardiol1991;18:657–662.2. Udvarhelyi IS, Gatsonis C, Epstein AM, Pashos CL, Newhouse JP, McNeil BJ.Acute myocardial infarction in the Medicare population: process of care andclinical outcomes.JAMA 1992;268:2530–2536.3. Goldberg RJ, McCormick D, Gurwitz JH, Yarzebski J, Lessard D, Gore JM.Age-related trends in short- and long-term survival after acute myocardialinfarction: a 20-year population-based perspective (1975–1995).Am J Cardiol1998;82:1311–1317.4. Smith SC, Gilpin E, Ahnve S, Dittrich H, Nicod P, Henning H, Ross J. Outlookafter acute myocardial infarction in the very elderly compared with that inpatients aged 65 to 75 years.J Am Coll Cardiol1990;16:784–792.5. Maggioni AP, Maseri A, Fresco C, Franziosi MG, Mauri F, Santoro E,Tognoni G. Age-related increase in mortality among patients with first myocar-dial infarctions treated with thrombolysis.N Engl J Med1993;329:1442–1448.6. Barakat K, Wilkinson P, Deaner A, Fluck D, Ranjadayalan K, Timmis A. How

should age affect management of acute myocardial infarction? A prospectivecohort study.Lancet1999;353:955–959.7. Himbert D, Steg PG, Juliard JM, Neukirch F, Aumont MC, Gourgon R.Eligibility for reperfusion therapy and outcome in elderly patients with acutemyocardial infarction.Eur Heart J1994;15:483–488.8. Bueno H, Lopez-Palop R, Perez-David E, Garcia-Garcia J, Lopez-Sendon JL,Delcan JL. Combined effect of age and right ventricular involvement on acuteinferior myocardial infarction prognosis.Circulation 1998;98:1714–1720.9. White HD, Barbash GI, Califf RM, Simes RJ, Granger CB, Weaver WD,Kleiman NS, Aylward PE, Gore JM, Vahanian A, Lee KL, Ross AM, Topol EJ.Age and outcome with contemporary thrombolytic therapy: results from theGUSTO-I trial.Circulation 1996;94:1826–1833.10. Holmes DR, White HD, Pieper KS, Ellis SG, Califf RM, Topol EJ. Effect ofage on outcome with primary angioplasty versus thrombolysis.J Am Coll Cardiol1999;33:412–419.11. Lee TC, Laramee LA, Rutherford BD, McConahay DR, Johnson WL, GiorgiLV, Ligon RW, Hartzler GO. Emergency percutaneous transluminal coronaryangioplasty for acute myocardial infarction in patients 70 years of age and older.Am J Cardiol1990;66:663–667.12. Barron HV, Bowlby LJ, Breen T, Rogers WJ, Canto JG, Zhang Y, Tiefen-brunn AJ, Weaver WD. Use of reperfusion therapy for acute myocardial infarc-tion in the United States: data from the National Registry of Myocardial Infarc-tion 2 [clinical investigation and reports].Circulation 1998;97:1150–1156.13. Fibrinolytic Therapy Trialists’ (FTT) Collaborative Group. Indications forfibrinolytic therapy in suspected acute myocardial infarction: collaborative over-view of early mortality and major morbidity results from all randomised trials ofmore than 1000 patients.Lancet1994;343:311–322.14. Gurwitz JH, Gore JM, Goldberg RJ, Barron HV, Breen T, Rundle AC, SloanMA, French W, Rogers WJ. Risk for intracranial hemorrhage after tissue plas-minogen activator treatment for acute myocardial infarction.Ann Intern Med1998;129:597–604.15. Lew AS, Hod H, Cercek B, Shah PK, Ganz W. Mortality and morbidity ratesof patients older and younger than 75 years with acute myocardial infarctiontreated with intravenous streptokinase.Am J Cardiol1987;59:1–5.16. Brower RW, Arnold AE, Lubsen J, Verstraete M, on behalf of the EuropeanCooperative Study Group for Recombinant Tissue-Type Plasminogen Activator.Coronary patency after intravenous infusion of recombinant tissue-type plasminogenactivator in acute myocardial infarction.J Am Coll Cardiol1988;11:681–688.17. Gruppo Italiano per lo Studio della Streptochinasi nell’Infarto Miocardico(GISSI). Long-term effects of intravenous thrombolysis in acute myocardialinfarction: final report of the GISSI study.Lancet1987;2:871–874.18. Thiemann DR, Coresh J, Schulman SP, Gerstenblith G, Oetgen WJ, PoweNR. Lack of benefit for intravenous thrombolysis in patients with myocardialinfarction who are older than 75 years.Circulation 2000;101:2239–2246.19. Laster SB, Rutherford BD, Giorgi LV, Shimsak TM, McConahay DR, JohnsonWL, Huber K, Ligon RW, Hartzler GO. Results of direct percutaneous transluminalcoronary angioplasty in octogenarians.Am J Cardiol1996;77:10–13.20. De Gregorio J, Kobayashi Y, Albiero R, Reimers B, DiMario C, Finci L,Colombo A. Coronary artery stenting in the elderly: short-term outcome and long-term angiographic and clinical follow-up.J Am Coll Cardiol1998;32:577–583.

Effect of Patency from Coronary Angioplasty DuringAcute Myocardial Infarction on Left Ventricular

Remodeling and Levels of Natriuretic Peptides Later

Yuji Hara, MD, Mareomi Hamada, MD, Yuji Shigematsu, MD, Tomoaki Ohtsuka, MD,Go Hiasa, MD, Akiyoshi Ogimoto, MD, Hideyuki Saeki, MD, Shigeru Nakata, RT, and

Kunio Hiwada, MD

Patency of the infarct-related artery is the mostimportant predictor of late survival of patients

after acute myocardial infarction (AMI).1 Myocardialreperfusion in AMI has been shown to result in a

reduction in left ventricular (LV) volume. Recentstudies have indicated that late coronary angioplastyimproves regional wall motion abnormalities and at-tenuates LV remodeling.2,3 In this study, we evaluatedwhether coronary angioplasty in patients with AMIreduced LV volume and decreased myocardial dam-age, and we measured plasma levels of atrial (ANP)and brain (BNP) natriuretic peptides.

• • •

Patients diagnosed with a first AMI were studiedprospectively. Study inclusion criteria were (1) diag-

From The Second Department of Internal Medicine, and The Depart-ment of Radiology, Ehime University School of Medicine, Ehime,Japan. Dr. Hara’s address is: The Second Department of InternalMedicine, Ehime University School of Medicine, Shigenobu-cho, On-sen-gun, Ehime 791-0295, Japan. E-mail: [email protected] received January 23, 2001; revised manuscript receivedand accepted May 11, 2001.

683©2001 by Excerpta Medica, Inc. All rights reserved. 0002-9149/01/$–see front matterThe American Journal of Cardiology Vol. 88 September 15, 2001 PII S0002-9149(01)01817-3