Atherosclerotic cardiovascular disease results in >19 million deaths annually, and coronary heart disease accounts for the majority of this toll. Despite major advances in treatment of coronary heart disease patients, a large number of victims of the disease who are apparently healthy die suddenly without prior symptoms. Available screening and diagnostic methods are insufficient to identify the victims before the event occurs. The recognition of the role of the vulnerable plaque has opened new avenues of opportunity in the field of cardiovascular medicine. This consensus document concludes the following. (1) Rupture-prone plaques are not the only vulnerable plaques. All types of atherosclerotic plaques with high likelihood of thrombotic complications and rapid progression should be considered as vulnerable plaques. We propose a classification for clinical as well as pathological evaluation of vulnerable plaques. (2) Vulnerable plaques are not the only culprit factors for the development of acute coronary syndromes, myocardial infarction, and sudden cardiac death. Vulnerable blood (prone to thrombosis) and vulnerable myocardium (prone to fatal arrhythmia) play an important role in the outcome. Therefore, the term "vulnerable patient" may be more appropriate and is proposed now for the identification of subjects with high likelihood of developing cardiac events in the near future. (3) A quantitative method for cumulative risk assessment of vulnerable patients needs to be developed that may include variables based on plaque, blood, and myocardial vulnerability. In Part I of this consensus document, we cover the new definition of vulnerable plaque and its relationship with vulnerable patients. Part II of this consensus document focuses on vulnerable blood and vulnerable myocardium and provide an outline of overall risk assessment of vulnerable patients. Parts I and II are meant to provide a general consensus and overviews the new field of vulnerable patient. Recently developed assays (eg, C-reactive protein), imaging techniques (eg, CT and MRI), noninvasive electrophysiological tests (for vulnerable myocardium), and emerging catheters (to localize and characterize vulnerable plaque) in combination with future genomic and proteomic techniques will guide us in the search for vulnerable patients. It will also lead to the development and deployment of new therapies and ultimately to reduce the incidence of acute coronary syndromes and sudden cardiac death. We encourage healthcare policy makers to promote translational research for screening and treatment of vulnerable patients.

/pdf/from-vulnerable-plaque-to-vulnerable-patient-a-call-for-new-47rrnyxj2m.pdf

From vulnerable plaque to vulnerable patient: a call for new definitions and risk assessment strategies: Part II.

It is important that the medical profession play a central role in critically evaluating the use of diagnostic procedures and therapies introduced and tested for detection, management, or prevention of disease. Rigorous, expert analysis of the available data documenting absolute and relative

/pdf/acc-aha-2008-guidelines-for-the-management-of-adults-with-4oqjti8ewr.pdf

ACC/AHA 2008 guidelines for the management of adults with congenital heart disease: Executive summary - A report of the American College of Cardiology/American Heart Association Task Force on practice guidelines (writing committee to develop guidelines for the management of adults with congenital heart disease)

https://www.hefssa.org/images/uploads/acc_aha_guidelines_for_adults_with_chd.pdf

ACC/AHA 2008 Guidelines for the Management of Adults With Congenital Heart Disease

Background: A substantial proportion of patients receiving fibrinolytic therapy for myocardial infarction with ST-segment elevation have inadequate reperfusion or reocclusion of the infarct-related artery, leading to an increased risk of complications and death. Methods: We enrolled 3491 patients, 18 to 75 years of age, who presented within 12 hours after the onset of an ST-elevation myocardial infarction and randomly assigned them to receive clopidogrel 8300-mg loading dose, followed by 75 mg once daily) or placebo. Patients received a fibrinolytic agent, aspirin, and when appropriate, heparin (dispensed according to body weight) and were echeduled to undergo angiography 48 to 192 hours after the start of study medication. The primary efficacy end point was a composite of an ocluded infarct-related artery (defined by a Thrombolysus in Myocardial Infarction flow grade of 0 or 1) on angiography or death or recurrent myocardial infarction before angiography. Results: The rates of the primary efficacy end point were 21.7 percent in the placebo group and 15.0 percent in the clopidogrel group, representing an absolute reduction of 6.7 percentage points in the rate and a 36 percent reduction in the odds of the end point with clopidogrel therapy (95 percent confidence interval, 24 to 47 percent; P<0.001). By 30 days, clopidogrel therapy reduced the odds ol the composite end point of death from cardiovascular causes, recurrent myocardial infarction, or recurrent ischemia leading to the need for urgent revascularization by 20 percent (from 14.1 to 11.6 percent, P=0.03). The rates of major bleeding and intracranial hemorrhage were similar in the two groups. Conclusions: In patients 75 years of age or younger who have myocardial infarction with ST-segment elevation and who receive aspirin and a standard fibrinolytic regimen, the addition of clopidogrel improves the patency rate of the infarct-related artery and reduces ischemic complications.

Addition of clopidogrel to aspirin and fibrinolytic therapy for myocardial infarction with ST-segment elevation

2021 ACC/AHA/SCAI Guideline for Coronary Artery Revascularization

The hemodynamic effects of 7 min i.v. flecainide were examined in rats with postischemic left ventricular dysfunction. For quantification of contractile function the isovolumic left ventricular pressure generating capacity and dp/dtmax were determined. Fifteen min after infusion the isovolumic maximum pressure was reduced for 33 mm Hg after flecainide (2 mg/kg; n = 12), whereas in the controls only a minimal reduction (12 mm Hg; n = 13) was found; dp/dtmax was also significantly reduced after flecainide. The results indicate - in contrast to prior investigations on normal hearts - a considerable negative action of 2 mg/kg flecainide i.v. on postischemic myocardium with reduced contractile function.

[Negative inotropic effect of flecainide on the post-ischemic heart with limited contractile function].

103. Coagulation and fibrinolysis in patients with acute coronary syndromes in the follow up

We investigated whether there is a relationship between the prolonged dysfunction after myocardial ischaemia and the postischaemic phosphocreatine overshoot phenomenon. In 16 open-chest rats 3 periods of 4 minutes of oxygen deficiency were performed and basal haemodynamic variables and the myocardial oxygen demand were determined during the recovery period. At the end of the 20 minutes recovery period, left ventricular pressure, dp/dtmax, ejection fraction, and myocardial oxygen demand were completely recovered. High energy phosphate levels, however, were still altered. The sum of adeninenucleotides was decreased to 78 ± 4% of control (\( (\overline x \pm \)SEM, p<0.05) . The level of phosphocreatine was markedly elevated to 162 ± 14 (\( (\overline x \pm \) SEM). The persistence of the phosphocreatine overshoot phenomenon, while basal function was already normalized, indicates that a reduced function and thus a reduced energy demand of the contractile apparatus are not the cause of the phosphocreatine overshoot. We found no close relationship between high energy levels and basal function or oxygen demand in myocardium after mild oxygen deficiency.

Phosphocreatine and adeninenucleotides in postasphyxial hearts with normal basal function and normal oxygen demand

We investigated the leucocyte-elastase and the activity of the kallikrein system including kinin precursors and plasma inhibition levels in 14 patients with unstable angina pectoris (normal or only slightly elevated creatinine kinase levels; no transmural myocardial infarction) and compared them with 10 controls. Leucocyte-elastase levels and activity of the kallikrein system were significantly elevated in unstable angina pectoris. The bradykinin precursor high-molecular-weight kininogen was markedly decreased to 79 +/- 16% indicating kinin generation. Except for a slight decrease in the beta factor XIIa inhibition, we observed no abnormalities in the plasma kallikrein inhibition or in the antithrombin III levels in patients with unstable angina pectoris. The findings indicate a significant activation of the plasma kallikrein-kinin system, which is not associated with a considerable reduction in the plasma inhibitor levels. Kinin generation might influence vascular tone and leucocyte function and thus be involved in the pathophysiologic alterations occurring in patients with recurrent angina at rest.

Activation of leukocytes and of the kallikrein‐kinin system in patients with unstable angina pectoris

P2724Inhospital mortality in patients with infarct-relaled cardiogenic shock undergoing coronary angiography treated with and without acute revascularization therapy

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