Speciality
Spotlight

 




 


Cardiology


 


   











Myocardial Infarction after Noncardiac Surgery

      

  • Badner NH, Knill RL, Brown JE, et al


    Myocardial Infarction After Noncardiac Surgery


    Anesthesiology 88: 572-578, 1998

      


    Postoperative myocardial infarction [PMI] in patients undergoing noncardiac surgery is an important source of morbidity and mortality. To better understand the occurrence of PMI in an at-risk population, cardiac enzymes, ECGs and clinical outcome were monitored prospectively in a group of noncardiac surgery patients with ischemic heart disease for the first 7 postoperative days [PODs].

      


    The study group consisted of 323 patients aged at least 50 years, with ischemic heart disease who underwent noncardiac surgery. Patients had daily clinical, ECG, and enzyme studies for seven PODs.

      


    Of the 323 patients, 18 had PMI [5.6%] and 17% of these were fatal. Only 3 of the 18 had chest pain and 10 had other symptoms. Most of the PMIs occurred on day 1 and all by day 4. Only 6 of the 18 had Q wave patterns on ECG.

      


    This group of patients with ischemic heart disease undergoing noncardiac surgery was extensively monitored for 7 postoperative days and showed 5.6% incidence of postoperative myocardial infarction which occurred in the early days and had no association with chest pain or Q waves on ECG

      


Myocardial Infarction

     

  • Leo Hofstra, Ing Han Liem et al

    Visualisation of cell death in vivo in patients with acute myocardial infarction

    Lancet, vol.356, July 15, 2000, pg. 209-212.

      

    In patients with acute myocardial infarction, cardiomyocyte death occurs in the infarct area. Animal studies have shown that ischemia of heart, followed by reperfusion, results in substantial loss of cardiomyocytes through apoptosis (programmed cell death). DNA fragmentation- a hallmark of apoptosis has been shown in cardiac biopsy samples obtained from patients with acute MI. An early event in apoptosis is externalization of phosphatidylserine from inner leaflet of plasma membrane to outer leaflet. The authors have shown that labelled annexin-V, which has a high affinity for phosphatidylserine is a specific and reliable tool for detection of apoptic cells- during ischemia and reperfusion in the murine heart. On the basis of these studies, authors have tested radionuclide imaging with technetium-99m-labelled human recombinant annexin-V to visualize cardiac cell death after reperfusion therapy in patients with an acute MI.

        

    Seven patients with an acute MI and 1 control were studied. All patients were treated with percutaneous transluminal coronary angioplasty. SPECT images of the heart were obtained after injecting I.V. 1mg of annexin V labelled with Tc-99m 2 hours after reperfusion. Routine myocardial resting-perfusion imaging was also done to verify infarct localisation.

        

    Interpretation of the study was that there was increased uptake of Tc-99m labelled annexin-V in the infarcted area of patients with an acute MI, suggesting that programmed cell death occurs in that area. This imaging technique may allow study of dynamics of reperfusion induced cell death in the area at risk and may help to assess interventions that inhibit cell death in patients with an acute MI.

         

    Editors’ comments :

    Radioimaging to identify myocardial cell death and probably injury.

        

    An imaging technique that identifies cell damage rapidly could facilitate clinical decision making. Although at least 3 hrs was required for radioannexin to be localised in Hofstra and colleagues’ study, improvement in radiopharmaceutical may permit more rapid imaging . Non-invasive targeting of apoptosis and stress induced externalisation of phosphatidylserine will lead to development of drugs and other treatments for increasing salvage of myocardium.

       
  • James A Goldstein, Demetris Demetriou et al

    Multiple complex coronary plaques in patients with acute myocardial infarction.

    New Eng J Med. Vol.343, Sept.28, 2000, pg.915-922

       

    Acute myocardial infarction is believed to be caused by rupture of an unstable coronary artery plaque that appears as a single lesion on angiography. Plaque instability may be caused by processes such as inflammation that exert adverse effects throughout the coronary vasculature and result in multiple unstable lesions.

       

    The authors analysed angiograms from 253 patients for complex coronary plaques characterised by thrombus, ulceration, plaque irregularity and impaired flow.

       

    They conclude that patients with acute myocardial infarction may have multiple complex coronary plaques that are associated with adverse clinical outcomes. Plaque instability may be due to a widespread process throughout the coronary vessels.

      

Myocardial Injury

     

  • D M Yellon, G F Baxter (Hatter Institute, Department of Academic and Clinical Cardiology, University College Hospital, London, UK)

    Sodium-hydrogen exchange in myocardial reperfusion injury.

    The Lancet vol.356, August 12, 2000, p.522-523

         

    Infarct size and reperfusion injury determine outcome after myocardial infarction (MI). There is need for therapy that will slow rate of ischaemic injury but also ‘buy time’ until reperfusion is started and limit the extent of lethal reperfusion injury. It has been recognised in the past few years, that the sodium/hydrogen exchange (NHE) mechanism may contribute to both ischaemic and reperfusion injury. NHE extrudes H+ from cells, thereby protecting them from acidosis. There are 6 isoforms of NHE, NHE-1 is the main one expressed on the sarcolemma of the myocyte.

         

    During ischaemia, myocyte NHE is activated and it removes intracellular H+ in exchange for Na+. Since Na+/K+ exchange does not function during ischaemia, accumulating intracelluar Na+ stimulates increased CA++ influx through the Na+/CA+ exchanger mechanism leading to intracellular Ca++ overload. Several NHE inhibitors have been developed to block these potentially lethal consequences. Most of these compounds are amiloride derivatives including cariporide and eniporide. In preclinial studies, their use has not shown consistent efficacy in reducing infarct size, when they are given after coronary occlusion or immediately before reperfusion.

        

    Since NHE inhibitors are clearly protective in laboratory animals when used before onset of ischaemia, it would be appropriate to concentrate on their use as pre-ischaemic treatments – e.g. before coronary artery bypass grafting (CABG) or in patients at potential risk of infarction, such as those with unstable angina. The evidence for their efficacy when given before reperfusion is not yet convincing. 

        

    In a large combined phase 2 and phase 3 trial (11500 patients) in which cariporide at 3 doses was assessed in patients judged to be at risk of MI, only in coronary artery bypass grafting group and with highest dose of cariporide, was any statistically significant benefit observed.

        

    Carefully designed preclinical studies are required to assess the contribution that reperfusion and ischaemic injury each makes to myocardial damage after MI. Only then the importance eof NHE inhibition as an adjunct therapy in acute MI can be determined in large and well-designed clinical studies, in which the dose and timing of drug treatment are rationally chosen.

        

Myocardial Laser Vascularisation

    

  • Stephen N Oesterle, Timothy A Sanborn et al (Division of Cardiology, Massachusetts General Hospital, USA)

    Percutaneous transmyocardial laser revascularisation for severe angina: the PACIFIC randomised trial.

    The Lancet Vol.356, November 18, 2000, pg.1705-1710.

         

    Percutaneous transmyocardial laser revascularisation (PTMR) is a proposed catheter-based therapy for refractory angina pectoris when bypass surgery or angioplasty is not possible. This is a randomised trial to assess the safety and efficacy of this technique.

         

    Two hundred twenty-one patients with reversible ischaemia of Canadian Cardiovascular Society angina class III or IV and incomplete response to other therapies were recruited. They were randomly assigned
    to PTMR with a holmium: YAG laser plus continued medical treatment or continued
    medical treatment only. Primary end-point was the exercise tolerance at 12 months.

        

    PTMR was associated withincreased exercise toelrance, low morbidity, lower angina scores and improved quality of life. There is controversy about mechanism of action and contribution of placebo effect cannot be quantified. This study suggests that that palliative procedure of PTMR provides some clinical benefits in the defined population of patients.

        




 

 

Speciality Spotlight

 

   

Myocardial Infarction after Noncardiac Surgery
      

  • Badner NH, Knill RL, Brown JE, et al
    Myocardial Infarction After Noncardiac Surgery
    Anesthesiology 88: 572-578, 1998
      
    Postoperative myocardial infarction [PMI] in patients undergoing noncardiac surgery is an important source of morbidity and mortality. To better understand the occurrence of PMI in an at-risk population, cardiac enzymes, ECGs and clinical outcome were monitored prospectively in a group of noncardiac surgery patients with ischemic heart disease for the first 7 postoperative days [PODs].
      
    The study group consisted of 323 patients aged at least 50 years, with ischemic heart disease who underwent noncardiac surgery. Patients had daily clinical, ECG, and enzyme studies for seven PODs.
      
    Of the 323 patients, 18 had PMI [5.6%] and 17% of these were fatal. Only 3 of the 18 had chest pain and 10 had other symptoms. Most of the PMIs occurred on day 1 and all by day 4. Only 6 of the 18 had Q wave patterns on ECG.
      
    This group of patients with ischemic heart disease undergoing noncardiac surgery was extensively monitored for 7 postoperative days and showed 5.6% incidence of postoperative myocardial infarction which occurred in the early days and had no association with chest pain or Q waves on ECG
      

Myocardial Infarction
     

  • Leo Hofstra, Ing Han Liem et al
    Visualisation of cell death in vivo in patients with acute myocardial infarction
    Lancet, vol.356, July 15, 2000, pg. 209-212.
      
    In patients with acute myocardial infarction, cardiomyocyte death occurs in the infarct area. Animal studies have shown that ischemia of heart, followed by reperfusion, results in substantial loss of cardiomyocytes through apoptosis (programmed cell death). DNA fragmentation- a hallmark of apoptosis has been shown in cardiac biopsy samples obtained from patients with acute MI. An early event in apoptosis is externalization of phosphatidylserine from inner leaflet of plasma membrane to outer leaflet. The authors have shown that labelled annexin-V, which has a high affinity for phosphatidylserine is a specific and reliable tool for detection of apoptic cells- during ischemia and reperfusion in the murine heart. On the basis of these studies, authors have tested radionuclide imaging with technetium-99m-labelled human recombinant annexin-V to visualize cardiac cell death after reperfusion therapy in patients with an acute MI.
        
    Seven patients with an acute MI and 1 control were studied. All patients were treated with percutaneous transluminal coronary angioplasty. SPECT images of the heart were obtained after injecting I.V. 1mg of annexin V labelled with Tc-99m 2 hours after reperfusion. Routine myocardial resting-perfusion imaging was also done to verify infarct localisation.
        
    Interpretation of the study was that there was increased uptake of Tc-99m labelled annexin-V in the infarcted area of patients with an acute MI, suggesting that programmed cell death occurs in that area. This imaging technique may allow study of dynamics of reperfusion induced cell death in the area at risk and may help to assess interventions that inhibit cell death in patients with an acute MI.
         
    Editors’ comments :
    Radioimaging to identify myocardial cell death and probably injury.
        
    An imaging technique that identifies cell damage rapidly could facilitate clinical decision making. Although at least 3 hrs was required for radioannexin to be localised in Hofstra and colleagues’ study, improvement in radiopharmaceutical may permit more rapid imaging . Non-invasive targeting of apoptosis and stress induced externalisation of phosphatidylserine will lead to development of drugs and other treatments for increasing salvage of myocardium.
       
  • James A Goldstein, Demetris Demetriou et al
    Multiple complex coronary plaques in patients with acute myocardial infarction.
    New Eng J Med. Vol.343, Sept.28, 2000, pg.915-922
       
    Acute myocardial infarction is believed to be caused by rupture of an unstable coronary artery plaque that appears as a single lesion on angiography. Plaque instability may be caused by processes such as inflammation that exert adverse effects throughout the coronary vasculature and result in multiple unstable lesions.
       
    The authors analysed angiograms from 253 patients for complex coronary plaques characterised by thrombus, ulceration, plaque irregularity and impaired flow.
       
    They conclude that patients with acute myocardial infarction may have multiple complex coronary plaques that are associated with adverse clinical outcomes. Plaque instability may be due to a widespread process throughout the coronary vessels.
      

Myocardial Injury
     

  • D M Yellon, G F Baxter (Hatter Institute, Department of Academic and Clinical Cardiology, University College Hospital, London, UK)
    Sodium-hydrogen exchange in myocardial reperfusion injury.
    The Lancet vol.356, August 12, 2000, p.522-523
         
    Infarct size and reperfusion injury determine outcome after myocardial infarction (MI). There is need for therapy that will slow rate of ischaemic injury but also ‘buy time’ until reperfusion is started and limit the extent of lethal reperfusion injury. It has been recognised in the past few years, that the sodium/hydrogen exchange (NHE) mechanism may contribute to both ischaemic and reperfusion injury. NHE extrudes H+ from cells, thereby protecting them from acidosis. There are 6 isoforms of NHE, NHE-1 is the main one expressed on the sarcolemma of the myocyte.
         
    During ischaemia, myocyte NHE is activated and it removes intracellular H+ in exchange for Na+. Since Na+/K+ exchange does not function during ischaemia, accumulating intracelluar Na+ stimulates increased CA++ influx through the Na+/CA+ exchanger mechanism leading to intracellular Ca++ overload. Several NHE inhibitors have been developed to block these potentially lethal consequences. Most of these compounds are amiloride derivatives including cariporide and eniporide. In preclinial studies, their use has not shown consistent efficacy in reducing infarct size, when they are given after coronary occlusion or immediately before reperfusion.
        
    Since NHE inhibitors are clearly protective in laboratory animals when used before onset of ischaemia, it would be appropriate to concentrate on their use as pre-ischaemic treatments – e.g. before coronary artery bypass grafting (CABG) or in patients at potential risk of infarction, such as those with unstable angina. The evidence for their efficacy when given before reperfusion is not yet convincing. 
        
    In a large combined phase 2 and phase 3 trial (11500 patients) in which cariporide at 3 doses was assessed in patients judged to be at risk of MI, only in coronary artery bypass grafting group and with highest dose of cariporide, was any statistically significant benefit observed.
        
    Carefully designed preclinical studies are required to assess the contribution that reperfusion and ischaemic injury each makes to myocardial damage after MI. Only then the importance eof NHE inhibition as an adjunct therapy in acute MI can be determined in large and well-designed clinical studies, in which the dose and timing of drug treatment are rationally chosen.
        

Myocardial Laser Vascularisation
    

  • Stephen N Oesterle, Timothy A Sanborn et al (Division of Cardiology, Massachusetts General Hospital, USA)
    Percutaneous transmyocardial laser revascularisation for severe angina: the PACIFIC randomised trial.
    The Lancet Vol.356, November 18, 2000, pg.1705-1710.
         
    Percutaneous transmyocardial laser revascularisation (PTMR) is a proposed catheter-based therapy for refractory angina pectoris when bypass surgery or angioplasty is not possible. This is a randomised trial to assess the safety and efficacy of this technique.
         
    Two hundred twenty-one patients with reversible ischaemia of Canadian Cardiovascular Society angina class III or IV and incomplete response to other therapies were recruited. They were randomly assigned to PTMR with a holmium: YAG laser plus continued medical treatment or continued medical treatment only. Primary end-point was the exercise tolerance at 12 months.
        
    PTMR was associated withincreased exercise toelrance, low morbidity, lower angina scores and improved quality of life. There is controversy about mechanism of action and contribution of placebo effect cannot be quantified. This study suggests that that palliative procedure of PTMR provides some clinical benefits in the defined population of patients.
        

 

By |2022-07-20T16:42:26+00:00July 20, 2022|Uncategorized|Comments Off on Myocardial

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