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Prognostic significance of serial rest and exercise radionoclide angiography after acute myocardial infarction
ABSTRACTS
SERIAL PLATELET RESPONSIVENESS TO ABACRADONIC ACID IN ACUTE MYOCABDIAL INFARCTION William T. Maddox, MD; Huey G. McDaniel, MD; Man-Chiu Poon. _ MD:_ and Charles E. Backlev. __ MD. FACC. University of Alabama and Veterans Administration Medical Centers; Birmingham, Alabama.
MONDAY, APRIL 26, 1982 AM SELECTED CLINICAL STUDIES IN ACUTE MYOCARDIAL INFARCTION 10:30- 12:oo MYOCARDIAL INFARCTION AT A YOUNG AGE - ROLE OF CIGARETTE SMOKING. John A. Kennedy, FRCP; John D. HoArthur, FRCP; Henry J. Dargie, HRCP; David O'Neill, MRCP; A. David Cunningham, BSc, vlestern Infirmary, Glasgow, Scotland.
I
In a prospective study we have investigated the relationship between cigarette smoking, coronary arteriographic findings and re-infarction rate in 104 consecutive patients who were under 45 years of age at the time of first acute myocardial infarction (AMI). Coronary arteriography (CA) was carried out 3 months after infarction in 81 patients (78%). Reasons for omission of CA were early death (9). severe peripheral vascular disease, Poor LV function, diabetes and follow up losses. Multi-vessel disease (more than one vessel blocked or>%% stenosed) was present in 56% while 3% had single vessel disease and 7% had normal or insignificantly diseased vessels. Of the total group 91% were smokers and had a mean cigarette consumption of>30 per day. All 30 patients with single vessel disease were smokers while Patients who had never smoked were more likely to have multivessel disease (p-=0.025). There was no significant difference in re-infarction rate in the first 2 months after infarction for non smokers, smokers and those who stopped at the time of infarction (ex-smokers). However, in the first subsequent year re-infarction occurred in 7 of 42 persistent smokers (17%) while no re-infarctions occurred in the 24 ex-smokers (pcO.025). In those followed for 3 years r-e-infarction had occurred in 13 of .?j persistent smokers (52%) while none of 11 ex-smokers had re-infarcted (~-zO.O05). We conclude that among young patients with AM1 heavy cigarette smokers have a different distribution of coronary artery disease than non smokers and that the incidence of myocardial re3;;s;;ion can be significantly reduced by stopping .
THROMBOXANEA2 IN ACUTE MYOCARDIAL INFARCTION Paul Walinsky, MD; J. Bryan Smith, Ph.D; Allan M. Lefer, Ph.D: Mark Lebenthal. MD: Paul Urban.MD: Sheldon Goldberg; MD; Arnold Greenspin, MD, Thornis jefferson University, Philadelphia, PA Platelet activation and generation of thromboxane (T,) A2 may be involved in the pathophysiology of acute myocardial infarction (AMI). We evaluated 9 patients (PTS) with AMI for the presence of TxB2, the stable metabolite of T,A2. All PTS had transmural AMI diagnosed by ECG criteria. PTS were studied from 2-6 hours after the onset of pain. In 4 PTS, a single sample of venous blood was obtained. In 5 AMI PTS with 6 acute coronary events coronary thrombolysis was performed with streptokinase (STR). Samples were obtained from the right atrium before (B) STR, 5 minutes (5 min) after restoration of patency of the vessel and 1 hour (1 hr) after restoration of patency. The mean initial T,Bg concentration in all 9 AMI PTS was 1.03+0.16. In contrast in 9 other PTS admitted to R/O AMI,-’ cn whom AMI was not present,T,Bz was In the thrombolysis PTS sequential T,B2 undetectable. levels were (pmol/ml). B STR 5 min. 1 hr. 0.76+0.9 \ p
during the pathophysio-
Acute myocardial infarction (AMI) is associated with increased serum concentrations of arachadonic acid (AA) to levels capable of producing in vitro platelet aggregation, suggesting a physiologic role of AA induced aggregation during or following AMI. For this reason we evaluated 22 patients (pts) serially for platelet responsiveness to AA during the week immediately after AMI. Six of 7 pts studied within 4 hrs and 12 of 13 pts studied within 48 hrs of AMI had markedly depressed aggregation even to higher than physiologic concentrations of AA. The only pt that was not acutely hyporesponsive had documented spasm and delayed but normal eventual aggregation. Mean aggregation to 0.5 mM AA within the first 48 hrs of AMI was 15X, significantly lower than control aggregation of 63% (p
PF0XX!lXSICXIFI~OFSERI?U~TANDEXERfZISERADIC+ IKkZIDE'ANG1CGPAPHYAETERm MyocARDvLtINFARCrIoN Kenneth G. lubrris, M), Rz&rt M. Califf, ICI, Sebastian T. Pa-i, M), Pay A. MXinnis, Ph.D, R. Fdwarrl Coleman, MD, Frederickcohb,M),Dukeuniwsityand~4~s,~ham, N.C. !Ihepurpose of this study was to detemim the relationshipktweenserial ~tsofmstandexerciseventricular functionandpmgmsis afterqcxardial. infarction (MI). Aoznsecutive series of102 consentingpatientswitIxxltseriousnoncardiacdiseaseunde~trest and upright bicycle exercise mitigated radionuclide angiograpb 3 and 8 weeks af&rMt, and clinical evaluation at one year. Tk ejection fraction at rest (REF) and exercise (EXF) andthechangeinEF (AEF) fmnrestto exercisewreaxparable at3 and 8 weeks. 3weeks 8weeks Msandiffe?x?nce RE!F 44.6k15.8 46.W14.5 1.6028.1 Fx EF 46.8i16.4 50.2t15.4 1.4B7.1 1.8k7.6 AEF 2.7k8.1 1.126.2 of
Qle year after the following
MI, 32 patients d.txonstzated one or mxe events: 16 dea’&s, 9 nonfatal MI, 26
lxxzpitalizations for unstable anginaor cmonarybypass surgery,14 weretWH?~FCIVfor angina. Iogistic regressionanalysisd5mmstratedthatREFat3wzekswas the mst significant predictor of death (p = 0.01); mrtality VEls 7%, 12%, and 35% in patients with mF > 0.50, 0.30 to 0.49 arid < 0.30 respeztively. Five deaths occurred between 3and8weks;co nsqwntly PE!? at 8 weeks was a less significantpredictorofnmtality. The AEF franrestto e.xercisedidmtpredidmxtality, k&was themst iqxxtantpredictor of total events, p = 0.003. !mesedatainiicatethat mninmsiveemluationofventricular function atrestandexercise, 3wzeks followkq MIpmvidessignificantprognosticdataregardjngdeath and cardiwascularevents in the firstyear p&MI.
March 1982
The American Journal of CARDIOLOGY
Volume 49
901
SERIAL PLATELET RESPONSIVENESS TO ABACRADONIC ACID IN ACUTE MYOCABDIAL INFARCTION William T. Maddox, MD; Huey G. McDaniel, MD; Man-Chiu Poon. _ MD:_ and Charles E. Backlev. __ MD. FACC. University of Alabama and Veterans Administration Medical Centers; Birmingham, Alabama.
MONDAY, APRIL 26, 1982 AM SELECTED CLINICAL STUDIES IN ACUTE MYOCARDIAL INFARCTION 10:30- 12:oo MYOCARDIAL INFARCTION AT A YOUNG AGE - ROLE OF CIGARETTE SMOKING. John A. Kennedy, FRCP; John D. HoArthur, FRCP; Henry J. Dargie, HRCP; David O'Neill, MRCP; A. David Cunningham, BSc, vlestern Infirmary, Glasgow, Scotland.
I
In a prospective study we have investigated the relationship between cigarette smoking, coronary arteriographic findings and re-infarction rate in 104 consecutive patients who were under 45 years of age at the time of first acute myocardial infarction (AMI). Coronary arteriography (CA) was carried out 3 months after infarction in 81 patients (78%). Reasons for omission of CA were early death (9). severe peripheral vascular disease, Poor LV function, diabetes and follow up losses. Multi-vessel disease (more than one vessel blocked or>%% stenosed) was present in 56% while 3% had single vessel disease and 7% had normal or insignificantly diseased vessels. Of the total group 91% were smokers and had a mean cigarette consumption of>30 per day. All 30 patients with single vessel disease were smokers while Patients who had never smoked were more likely to have multivessel disease (p-=0.025). There was no significant difference in re-infarction rate in the first 2 months after infarction for non smokers, smokers and those who stopped at the time of infarction (ex-smokers). However, in the first subsequent year re-infarction occurred in 7 of 42 persistent smokers (17%) while no re-infarctions occurred in the 24 ex-smokers (pcO.025). In those followed for 3 years r-e-infarction had occurred in 13 of .?j persistent smokers (52%) while none of 11 ex-smokers had re-infarcted (~-zO.O05). We conclude that among young patients with AM1 heavy cigarette smokers have a different distribution of coronary artery disease than non smokers and that the incidence of myocardial re3;;s;;ion can be significantly reduced by stopping .
THROMBOXANEA2 IN ACUTE MYOCARDIAL INFARCTION Paul Walinsky, MD; J. Bryan Smith, Ph.D; Allan M. Lefer, Ph.D: Mark Lebenthal. MD: Paul Urban.MD: Sheldon Goldberg; MD; Arnold Greenspin, MD, Thornis jefferson University, Philadelphia, PA Platelet activation and generation of thromboxane (T,) A2 may be involved in the pathophysiology of acute myocardial infarction (AMI). We evaluated 9 patients (PTS) with AMI for the presence of TxB2, the stable metabolite of T,A2. All PTS had transmural AMI diagnosed by ECG criteria. PTS were studied from 2-6 hours after the onset of pain. In 4 PTS, a single sample of venous blood was obtained. In 5 AMI PTS with 6 acute coronary events coronary thrombolysis was performed with streptokinase (STR). Samples were obtained from the right atrium before (B) STR, 5 minutes (5 min) after restoration of patency of the vessel and 1 hour (1 hr) after restoration of patency. The mean initial T,Bg concentration in all 9 AMI PTS was 1.03+0.16. In contrast in 9 other PTS admitted to R/O AMI,-’ cn whom AMI was not present,T,Bz was In the thrombolysis PTS sequential T,B2 undetectable. levels were (pmol/ml). B STR 5 min. 1 hr. 0.76+0.9 \ p
during the pathophysio-
Acute myocardial infarction (AMI) is associated with increased serum concentrations of arachadonic acid (AA) to levels capable of producing in vitro platelet aggregation, suggesting a physiologic role of AA induced aggregation during or following AMI. For this reason we evaluated 22 patients (pts) serially for platelet responsiveness to AA during the week immediately after AMI. Six of 7 pts studied within 4 hrs and 12 of 13 pts studied within 48 hrs of AMI had markedly depressed aggregation even to higher than physiologic concentrations of AA. The only pt that was not acutely hyporesponsive had documented spasm and delayed but normal eventual aggregation. Mean aggregation to 0.5 mM AA within the first 48 hrs of AMI was 15X, significantly lower than control aggregation of 63% (p
PF0XX!lXSICXIFI~OFSERI?U~TANDEXERfZISERADIC+ IKkZIDE'ANG1CGPAPHYAETERm MyocARDvLtINFARCrIoN Kenneth G. lubrris, M), Rz&rt M. Califf, ICI, Sebastian T. Pa-i, M), Pay A. MXinnis, Ph.D, R. Fdwarrl Coleman, MD, Frederickcohb,M),Dukeuniwsityand~4~s,~ham, N.C. !Ihepurpose of this study was to detemim the relationshipktweenserial ~tsofmstandexerciseventricular functionandpmgmsis afterqcxardial. infarction (MI). Aoznsecutive series of102 consentingpatientswitIxxltseriousnoncardiacdiseaseunde~trest and upright bicycle exercise mitigated radionuclide angiograpb 3 and 8 weeks af&rMt, and clinical evaluation at one year. Tk ejection fraction at rest (REF) and exercise (EXF) andthechangeinEF (AEF) fmnrestto exercisewreaxparable at3 and 8 weeks. 3weeks 8weeks Msandiffe?x?nce RE!F 44.6k15.8 46.W14.5 1.6028.1 Fx EF 46.8i16.4 50.2t15.4 1.4B7.1 1.8k7.6 AEF 2.7k8.1 1.126.2 of
Qle year after the following
MI, 32 patients d.txonstzated one or mxe events: 16 dea’&s, 9 nonfatal MI, 26
lxxzpitalizations for unstable anginaor cmonarybypass surgery,14 weretWH?~FCIVfor angina. Iogistic regressionanalysisd5mmstratedthatREFat3wzekswas the mst significant predictor of death (p = 0.01); mrtality VEls 7%, 12%, and 35% in patients with mF > 0.50, 0.30 to 0.49 arid < 0.30 respeztively. Five deaths occurred between 3and8weks;co nsqwntly PE!? at 8 weeks was a less significantpredictorofnmtality. The AEF franrestto e.xercisedidmtpredidmxtality, k&was themst iqxxtantpredictor of total events, p = 0.003. !mesedatainiicatethat mninmsiveemluationofventricular function atrestandexercise, 3wzeks followkq MIpmvidessignificantprognosticdataregardjngdeath and cardiwascularevents in the firstyear p&MI.
March 1982
The American Journal of CARDIOLOGY
Volume 49
901