ΣΤΕΦΑΝΙΑΙΑ ΝΟΣΟΣ ΚΑΡΔΙΑΚΗ ΑΝΕΠΑΡΚΕΙΑ ΑΓΓΕΙΑΚΟ ΕΓΚΕΦΑΛΙΚΟ ΕΠΕΙΣΟΔΙΟ

Παρουσίαση με θέμα: "ΣΤΕΦΑΝΙΑΙΑ ΝΟΣΟΣ ΚΑΡΔΙΑΚΗ ΑΝΕΠΑΡΚΕΙΑ ΑΓΓΕΙΑΚΟ ΕΓΚΕΦΑΛΙΚΟ ΕΠΕΙΣΟΔΙΟ"— Μεταγράφημα παρουσίασης:

1 ΣΤΕΦΑΝΙΑΙΑ ΝΟΣΟΣ ΚΑΡΔΙΑΚΗ ΑΝΕΠΑΡΚΕΙΑ ΑΓΓΕΙΑΚΟ ΕΓΚΕΦΑΛΙΚΟ ΕΠΕΙΣΟΔΙΟ
ΣΤΕΦΑΝΙΑΙΑ ΝΟΣΟΣ ΚΑΡΔΙΑΚΗ ΑΝΕΠΑΡΚΕΙΑ ΑΓΓΕΙΑΚΟ ΕΓΚΕΦΑΛΙΚΟ ΕΠΕΙΣΟΔΙΟ Κωνσταντίνος Μακαρίτσης Επίκουρος Καθηγητής Παθολογίας Πανεπιστημίου Θεσσαλίας

2 ΣΤΕΦΑΝΙΑΙΑ ΝΟΣΟΣ

3 Leading Causes of Death for All Males and Females United States: 2001
A Total CVD B Cancer C Accidents D Chronic Lower Respiratory Diseases E Diabetes Mellitus F Alzheimer’s Disease p6 Source: CDC/NCHS.

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9 MAP = DBP + PULSE PRESSURE / 3
PULSE PRESSURE = SBP – DBP

10 Coronary heart disease (CHD) is the most common form of heart disease, the leading cause of death for Americans. About 12.6 million Americans suffer from CHD, which often results in a heart attack.   About 1.1 million Americans suffer a heart attack each year—about 515,000 of these heart attacks are fatal.

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19 Pharmacological dissolution of thrombus in infarct-related artery
  Pharmacological dissolution of thrombus in infarct-related artery. This figure shows a schematic view of a longitudinal section of an infarct-related artery at the level of the obstructive thrombus. Following rupture of a vulnerable plaque (bottom center), the coagulation cascade is activated, ultimately leading to the deposition of fibrin strands (blue curvilinear arcs); platelets are activated and begin to aggregate (transition from flat discs representing inactive platelets to green spiked ball elements representing activated and aggregating platelets). The mesh of fibrin strands and platelet aggregates obstructs flow (normally moving from left to right) in the infarct-related artery; this would correspond to TIMI grade 0 on angiography. Pharmacological reperfusion is a multipronged approach consisting of fibrinolytic agents that digest fibrin, antithrombins that prevent the formation of thrombin and inhibit the activity of thrombin that is formed, and antiplatelet therapy. (Courtesy of Luke Wells, The Exeter Group.)

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24 Schematic representation of the progression of myocardial necrosis after coronary artery occlusion. Necrosis begins in a small zone of the myocardium beneath the endocardial surface in the center of the ischemic zone. This entire region of myocardium (dashed outline) depends on the occluded vessel for perfusion and is the area at risk. Note that a very narrow zone of myocardium immediately beneath the endocardium is spared from necrosis because it can be oxygenated by diffusion from the ventricle. (From Schoen FJ: The heart. In Cotran RS, Kumar V, Collins T [eds]: Pathologic Basis of Disease. 6th ed. Philadelphia, WB Saunders, 1999, p 557.)

25 Thrombus propagation. A, Left anterior descending coronary artery cut open longitudinally, showing a dark (red) stagnation thrombosis propagating upstream from the initiating rupture/platelet-rich thrombus at the arrow. In this case,the thrombus has propagated proximally up to the nearest major side branch (the first diagonal branch). B, The right coronary artery cut open longitudinally, showing a huge stagnation thrombosis propagating downstream from the initiating rupture/platelet-rich thrombus at the arrow. Unlike upstream thrombus propagation, downstream propagation may, as in this case, occlude major side branches. c = contrast medium injected postmortem; O = coronary ostium. (From Falk E: Coronary thrombosis: Pathogenesis and clinical manifestations. Am J Cardiol 68:28B, 1991 Thrombus propagation. A, Left anterior descending coronary artery cut open longitudinally, showing a dark (red) stagnation thrombosis propagating upstream from the initiating rupture/platelet-rich thrombus at the arrow. In this case,the thrombus has propagated proximally up to the nearest major side branch (the first diagonal branch). B, The right coronary artery cut open longitudinally, showing a huge stagnation thrombosis propagating downstream from the initiating rupture/platelet-rich thrombus at the arrow. Unlike upstream thrombus propagation, downstream propagation may, as in this case, occlude major side branches. c = contrast medium injected postmortem; O = coronary ostium. (From Falk E: Coronary thrombosis: Pathogenesis and clinical manifestations. Am J Cardiol 68:28B, 1991.)

26 Acute myocardial infarction, predominantly of the posterolateral left ventricle, demonstrated histochemically by a lack of staining by the triphenyltetrazolium chloride (TTC) stain in areas of necrosis. The staining defect is due to the enzyme leakage that follows cell death. Note the myocardial hemorrhage at one edge of the infarct that was associated with cardiac rupture, and the anterior scar (lower left), indicative of old infarct. (Specimen oriented with posterior wall at top.) (From Schoen FJ: The heart. In Cotran RS, Kumar V, Collins T [eds]: Pathologic Basis of Disease. 6th ed. Philadelphia, WB Saunders, 1999, p 559.)

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28 A 47-year-old man with no prior history of cardiac disease presented to an outside hospital describing “ an awesome feeling that just sat in my chest” associated with bilateral arm weakness. The initial electrocardiogram (A) revealed STsegment elevation in the right precordial leads and to a lesser extent in the inferior leads.

29 The patient was treated with fibrinolytic therapy and transferred for catheterization. Angiography revealed a tight stenosis of a proximal nondominant right coronary artery (B, arrow) without significant disease in the left coronary artery.

30 Contrastenhanced cardiac magnetic resonance imaging (C) demonstrated delayed hyperenhancement consistent with injury of the right ventricle (RV) with distinct involvement of the right ventricular free wall (arrowhead), sparing the left ventricle (LV) as well as the right ventricular apex. The patient remained hemodynamically stable throughout his hospital course and was discharged home.

31 Nomenclature of acute coronary syndromes
Nomenclature of acute coronary syndromes. Patients with ischemic discomfort present with or without ST-segment elevation on the electrocardiogram (ECG). The majority of patients with ST-segment elevation ultimately develop a Q wave acute myocardial infarction (QwMI), whereas a minority develop a non-Q-wave myocardial infarction (NQMI). Patients who present without ST-segment elevation are either experiencing unstable angina or a non-ST-segment elevation myocardial infarction (NSTEMI). The distinction between these two diagnoses is ultimately made based on the presence or absence of a cardiac biomarker detected in the blood. Most patients with NSTEMI do not evolve a Q wave on the 12-lead ECG and are subsequently referred to as having sustained an NQMI; only a minority of NSTEMI patients develop a Q wave MI and are later diagnosed as Q wave MI. The spectrum of clinical conditions ranging from unstable angina to non-Q wave MI constitutes the acute coronary syndromes. (From Braunwald E, Antman EM, Beasley JW, et al: ACC/AHA guidelines for the management of patients with unstable angina: A report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines [Committee on the Management of Patients With Unstable Angina]. J Am Coll Cardiol 36:970, 2000

32 The kinetics of release of creatine kinase MB (CKMB) and cardiac troponin in patients who do not undergo reperfusion are shown in the solid green and red curves as multiples of the upper reference limit (URL). Note that when patients with ST-segment elevation myocardial infarction (STEMI) undergo reperfusion, as depicted in the dashed green and red curves, the cardiac biomarkers are detected sooner, rise to a higher peak value, but decline more rapidly, resulting in a smaller area under the curve and limitation of infarct size. AMI = acute myocardial infarction.

33 The zone of necrosing myocardium is shown at the top of the figure, followed in the middle portion of the figure by a diagram of a cardiomyocyte that is in the process of releasing biomarkers. Most troponin exists as a tripartite complex of C, I, and T components that are bound to actin filaments, although a small amount of troponin is free in the cytoplasm. After disruption of the sarcolemmal membrane of the cardiomyocyte, the cytoplasmic pool of troponin is released first (left-most arrow in bottom portion of figure), followed by a more protracted release from the disintegrating myofilaments that may continue for several days (three-headed arrow). Cardiac troponin levels rise to about 20 to 50 times the upper reference limit (the 99th percentile of values in a reference control group) in patients who have a “classic” acute myocardial infarction (MI) and sustain sufficient myocardial necrosis to result in abnormally elevated levels of the MB fraction of creatine kinase (CK-MB). Clinicians can now diagnose episodes of microinfarction by sensitive assays that detect cardiac troponin elevations above the upper reference limit, even though CK-MB levels may still be in the normal reference range (not shown). (From Antman EM: Decision making with cardiac troponin tests. N Engl J Med 346:2079, 2002.)

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35 Options for transportation of STEMI patients and initial reperfusion treatment. Reperfusion in patients with STEMI can be accomplished by the pharmacological (fibrinolysis) or catheter-based (primary PCI) approaches. Implementation of these strategies varies based on the mode of transportation of the patient and capabilities at the receiving hospital. A, Patient transported by emergency medical services (EMS) after calling 911. Transport time to the hospital is variable from case to case, but the goal is to keep total ischemic time less than 120 minutes. There are three possibilities. (1) If EMS has fibrinolytic capability and the patient qualifies for therapy, prehospital fibrinolysis should be started within 30 minutes of EMS arrival on scene. (2) If EMS is not capable of administering prehospital fibrinolysis and the patient is transported to a non-PCI capable hospital, the hospital door-to-needle time should be less than or equal to 30 minutes for patients in whom fibrinolysis is indicated. (3) If EMS is not capable of administering prehospital fibrinolysis and the patient is transported to a PCI-capable hospital, the hospital door-to-balloon time should be less than or equal to 90 minutes. Interhospital transfer: It is also appropriate to consider emergency interhospital transfer of the patient to a PCI-capable hospital for mechanical revascularization if (1) there is a contraindication to fibrinolysis; (2) PCI can be initiated promptly (≤90 min after the patient presented to the initial receiving hospital or ≤60 min compared to when fibrinolysis could be initiated at the initial receiving hospital; (3) fibrinolysis is administered and is unsuccessful (i.e., “ rescue PCI” ). Secondary nonemergency interhospital transfer can be considered for recurrent ischemia (B). Patient self-transport: Patient self-transportation is discouraged. If the patient arrives at a non-PCI-capable hospital, the door-to-needle time should be 30 minutes or less. If the patient arrives at a PCI-capable hospital, the door-to-balloon time should be 90 minutes or less. The treatment options and time recommendations after first hospital arrival are the same. B, For patients who receive fibrinolysis, noninvasive risk stratification is recommended to identify the need for rescue PCI (failed fibrinolysis) or ischemia drive PCI. Regardless of the initial method of reperfusion treatment, all patients should receive late hospital care and secondary prevention of STEMI. †The medical system goal is to facilitate rapid recognition and treatment of patients with STEMI such that door-to-needle (or EMS-to-needle) for initiation of fibrinolytic therapy can be achieved within 30 minutes or that door-to-balloon (or EMS-to-balloon) or PCI can be achieved within 90 minutes. These goals should not be understood as “ ideal” times, but rather the longest times that should be considered acceptable for a given system. Systems that are able to achieve even more rapid times for treatment of patients with STEMI should be encouraged. (Adapted from Armstrong PW, Collen D, Antman E: Fibrinolysis for acute myocardial infarction: The future is here and now. Circulation 107:2533, 2003; and Antman EM, et al: ACC/AHA Guidelines for the Management of Patients with ST-Elevation Myocardial Infarction, 2004 [

36 Management of patients with UA/NSTEMI

37 Algorithm for the management of patients with unstable angina or non-ST elevation myocardial infarction (UA/NSTEMI).

38 Algorithm for the management of lower risk patients with unstable angina or non-ST elevation myocardial infarction (UA/NSTEMI).

39 Algorithm for the management of medium and high risk patients with unstable angina or non-ST elevation myocardial infarction (UA/NSTEMI).

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44 Impact of left ventricular function on survival
following myocardial infarction

45 Hypokalemia and ventricular fibrillation in acute myocardial infarction

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56 Importance of time to reperfusion in patients receiving fibrinolytic therapy for ST segment elevation myocardial infarction. The data from 22 trials of fibrinolytic therapy were pooled and the findings stratified by the six time categories shown in the figure. The number of lives saved per 1000 patients treated with fibrinolytics compared with placebo is greatest the earlier treatment is initiated after the onset of symptoms and this decreases in a nonlinear fashion with incremental time delays. Since the life-saving effect of fibrinolysis is maximal in the first hour from onset of symptoms, this has been referred to as the “ golden hour” for pharmacological reperfusion. (From Boersma E, Maas AC, Deckers JW, et al: Early thrombolytic treatment in acute myocardial infarction: Reappraisal of the golden hour. Lancet 348:771, 1996.)

57 Mortality differences during days 0 to 35 subdivided by presentation features in a collaborative overview of results from nine trials of thrombolytic therapy. The absolute mortality rates are shown for fibrinolytic and control groups in the center portion of the figure for each of the clinical features at presentation listed on the left side of the figure. The ratio of the odds of death in the fibrinolytic group to that in the control group is shown for each subdivision (colored square), along with its 99 percent confidence interval (horizontal line). The summary odds ratio at the bottom of the figure corresponds to an 18 percent proportional reduction in 35-day mortality and is highly statistically significant. This translates to a reduction of 18 deaths per 1000 patients treated with thrombolytic agents. (From Fibrinolytic Therapy Trialists’ [FTT] Collaborative Group: Indications for fibrinolytic therapy in suspected acute myocardial infarction: Collaborative over­view of mortality and major morbidity results from all randomized trials of more than 1000 patients. Lancet 343:311, Copyright by The Lancet Ltd.)

58 Short-term clinical outcomes of patients in 23 randomized trials
of primary angioplasty versus thrombolysis

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60 Results of meta-analysis comparing primary stenting with primary balloon angioplasty. MACE = major adverse cardiac events including death, reinfarction, and target vessel revascularization (TVR)

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65 Algorithm for assessment of need for electrophysiological study and implantation of an implantable cardioverter-defibrillator (ICD) in ST segment elevation myocardial infarction (STEMI) patients without ventricular fibrillation (VF) or sustained ventricular tachycardia (VT) more than 72 hours after STEMI.  Algorithm for assessment of need for electrophysiological study and implantation of an implantable cardioverter-defibrillator (ICD) in ST segment elevation myocardial infarction (STEMI) patients without ventricular fibrillation (VF) or sustained ventricular tachycardia (VT) more than 72 hours after STEMI. The appropriate management path is selected based on the timing and measurement of left ventricular ejection fraction (EF) (see table at top of figure). EF measurements obtained 3 days or less after STEMI should be repeated before proceeding with the algorithm. In path A, patients with markedly depressed left ventricular function at least 1 month post-STEMI are referred for insertion of an ICD. Path B illustrates the management of patients in an intermediate-risk category who require further evaluation with an electrophysiology study (EPS). If the EPS reveals inducible ventricular tachycardia/ventricular fibrillation, an ICD is implanted; if the EPS is negative, no ICD is implanted and the patient receives medical therapy post-STEMI. Path C illustrates the management of patients with preserved left ventricular function who do not receive an ICD and are treated with medical therapy post-STEMI. LOE = level of evidence; NS-VT = nonsustained ventricular tachycardia. (From Antman EM, et al: ACC/AHA Guidelines for the Management of Patients with ST-Elevation Myocardial Infarction [

66 Effect of beta blockers on mortality rate in patients with myocardial infarction.
The relative risk of mortality is reduced with beta blockers both during the acute phase of treatment and when prescribed as secondary prevention after acute myocardial infarction.

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68 Effect of angiotensin-converting enzyme inhibitors on mortality after myocardial infarction: results from the long-term trials.

69 Effects of angiotensin-converting enzyme inhibitors on mortality after myocardial infarction: results from the short-term trials.

70 Effects of an angiotensin-converting enzyme inhibitor (captopril), angiotensin receptor blocker (valsartan), or the combination after myocardial infarction. The Kaplan-Meier estimates of mortality.

71 Effect of a selective aldosterone receptor blocker (eplerenone) after myocardial infarction. The Kaplan-Meier estimates of the rate of death from cardiovascular causes or hospitalization for cardiovascular events in the EPHESUS trial are depicted.

72 Mechanisms of action of antiplatelet therapies.
ADP=adenosine diphosphate; cAMP=cyclic adenosine monophosphate; COX=cyclooxygenase; GP=glycoprotein; TXA2=thromboxane A2

73 Benefit of the addition of clopidogrel to aspirin compared
with placebo and aspirin during the first 30 days

74 Benefit of the addition of clopidogrel to aspirin compared
with placebo and aspirin between 31 days and 1 year

75 ΚΑΡΔΙΑΚΗ ΑΝΕΠΑΡΚΕΙΑ

76 Definition of heart failure
AHA / ACC HF guidelines 2001 Clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood Clinical symptoms / signs secondary to abnormal ventricular function ESC HF guidelines 2001

77 • 6% - 10% of people > 65 years
HEART FAILURE The Problem (USA) • 5,000,000 patients • 6,500,000 hospital days / year • 300,000 deaths / year • 6% - 10% of people > 65 years • 5.4% of health care budget (38 billion) • Incidence x 2 in last ten years Gottdiener J et al. JACC 2000;35:1628 Haldeman GA et al. Am Heart J 1999;137:352 Kannel WB et al. Am Heart J 1991;121:951 O’Connell JB et al. J Heart Lung Transplant 1993;13:S107

78 Stages in the Evolution Clinical Characteristics
HEART FAILURE Hypertension Diabetes, Hyperchol. Family Hx Cardiotoxins A Stages in the Evolution of Heart Failure Clinical Characteristics B Heart disease (any) Asymptomatic LV dysfunction Systolic / Diastolic C Dyspnea, Fatigue Reduced exercise tolerance a insuficiencia cardiaca es el resultado del fracaso del tratamiento de las cardiopatias (no hay insuficiencia cardiaca sin cardiopatia) Sin embargo, el diagnostico de insuficiencia cardiaca es elusivo, no solo por la dificltad de su definicion sino porque ademas es un espectro continuo que comienza eante la rpesencia de factores de riesgo de cardiaopatia e insuficiencia cardiaca D Marked symptoms at rest despite max. therapy AHA / ACC HF guidelines 2001 4

79 HEART FAILURE 36 Direct Causes 1- Myocardial abnormalities (CHD!) 2- Hemodynamic overload 3- Ventricular filling abnormalities 4- Ventricular dyssynergy 5- Changes in cardiac rhythm Etiology of Heart Failure. Etiologic risk factors Direct causes of heart failure The direct cause of heart failure may be a change in any of the regulators of ventricular function: contractility, preload, afterload and heart rate. These primary causes may be classified into the following groups: myocardial changes, hemodynamic or mechanical abnormalities, abnormalities of ventricular filling, ventricular dyssynergy and changes in cardiac rhythm.

80 Aggravating Factors Medications New heart disease Myocardial ischemia
HEART FAILURE Aggravating Factors Medications New heart disease Myocardial ischemia Pregnancy Arrhythmias (AF) Infections Thromboembolism Hyper/hypothyroidism Endocarditis Obesity Hypertension Physical activity Dietary excess Treatment of Heart Failure. Correction of aggravating factors Often a lack of response to conventional therapy for heart failure is due to the presence of uncorrected aggravating or precipitating factors. It is important to always consider the possibility of such factors, particularly in cases of refractory failure. AF: atrial fibrillation.

81 Prognosis Cardiac Mortality % LVEF HEART FAILURE 50 Post MI n=196 40
202 Prognosis 50 <30 Post MI n=196 40 Cardiac Mortality % 30 31-35 20 Prognosis. Hemodynamic factors The ejection fraction of the left ventricle (LVEF) is one of the few objective and easily reproducible parameters which are closely related to prognosis. Even in patients with subclinical ventricular dysfunction, the decrease in LVEF implies a poor prognosis. In this slide, the relationship between LVEF and cardiac mortality in a group of patients post-myocardial infarction is shown. Note the exponential increase in mortality when the LVEF is less than 40%. An interesting finding is that pharmacologic interventions which improve prognosis in the subgroup of patients with severe depression of ventricular function do not serve the patients with asymptomatic ventricular dysfunction as well. This points up the important clinical role of defining the LVEF. Brodie B et al. Am J Cardiol 1992;69:1113 36-45 10 46-53 54-60 >60 80 70 60 50 40 30 20 Brodie B. et al Am J Cardiol 1992;69:1113 LVEF

82 HEART FAILURE SYMPTOMS
1Fatigue: most common presenting symptom secondary to decreased cardiac output to skeletal muscle. 2Dyspnea: secondary to pulmonary congestion when pulmonary venous pressure is greater than 20 mm Hg, which results in transudative leakage of fluid into the pulmonary parenchyma. 3Decreased mental acuity and urine output: result of diminished forward flow to cerebral and kidney circulation. 4Paroxysmal nocturnal dyspnea and orthopnea: fluid from gravity-dependent portions of body are redistributed into intravascular circulation when recumbent, resulting in increased intracardiac filling pressures. 5Abdominal distension: elevated right-sided filling pressures cause hepatic swelling and intestinal edema. pPeripheral edema and weight gain: fluid retention due to neuroendocrine mechanisms and elevated right-sided pressures cause accumulation of interstitial fluid.

83 HEART FAILURE SIGNS LEFT-SIDED HEART FAILURE
·   Cool extremities, mild cyanosis, and poor capillary refill secondary to poor cardiac output. ·   Tachycardia and tachypnea due to high sympathetic tone. · Cheyne-Stokes breathing: hyperventilation followed by temporary cessation of breathing due to increased circulation time between lungs and CNS respiratory centers. · Pulmonary ronchi and raIes occur if left atrial pressure is greater than 20 mm Hg. · Third heart sound occurs during early diastoIe, during rapid ventricular filling phase: suggestive of pathologic increase in diastolic ventricular fiIling due to fluid overIoad. · Fourth heart sound: produced by contraction of atria in late diastole and occurs when the atrial-augmented filIing enters a pathoIogically stiffened ventricle.

84 HEART FAILURE SIGNS RRIGHT-SIDED HEART FAILURE pPeripheraI edema
Elevated juguIar venous pulsation with prominent V wave and steep Y descent pPeripheraI edema Enlarged Iiver span from hepatic enlargement  Ascites hHepatojugular refIuχ

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86 ΧΑΜΗΛΗ ΚΑΡΔΙΑΚΗ ΠΑΡΟΧΗ Ή ΠΕΡΙΦΕΡΙΚΗ ΑΡΤΗΡΙΟΔΙΑΣΤΟΛΗ
ΝΕΦΡΙΚΗ ΑΓΓΕΙΟΣΥΣΠΑΣΗ ΝΕΦΡΙΚΗΣ ΠΙΕΣΗΣ ΔΙΗΘΗΣΕΩΣ α-ΑΔΡΕΝΕΡΓΙΚΗΣ ΔΡΑΣΤΗΡΙΟΤΗΤΑΣ ΔΡΑΣΤΗΡΙΟΤΗΤΑΣ ΑΓΓΕΙΟΤΑΣΙΝΗΣ ΙΙ ΡΥΘΜΟΥ ΣΠΕΙΡΑΜΑΤΙΚΗΣ ΔΙΗΘΗΣΗΣ ΕΠΑΝΑΡΡΟΦΗΣΗΣ ΝΑΤΡΙΟΥ ΚΑΙ ΥΔΑΤΟΣ ΣΤΟ ΕΓΓΥΣ ΣΥΓΚΕΝΤΡΩΣΗΣ ΝΑΤΡΙΟΥ ΚΑΙ ΥΔΑΤΟΣ ΣΤΟ ΑΠΩ ΑΠΟΥΣΙΑ ΦΑΙΝΟΜΕΝΟΥ ΔΙΑΦΥΓΗΣ ΑΝΤΙΣΤΑΣΗ ΣΤΑ ΝΑΤΡΙΟΥΡΗΤΙΚΑ ΠΕΠΤΙΔΙΑ

87 ΚΑΡΔΙΑΚΗ ΑΝΕΠΑΡΚΕΙΑ ΜΕ ΧΑΜΗΛΗ ΚΑΡΔΙΑΚΗ ΠΑΡΟΧΗ
ΚΑΡΔΙΑΚΗ ΑΝΕΠΑΡΚΕΙΑ ΜΕ ΥΨΗΛΗ ΚΑΡΔΙΑΚΗ ΠΑΡΟΧΗ ΚΑΡΔΙΑΚΗΣ ΠΑΡΟΧΗΣ ΠΕΡΙΦΕΡΙΚΩΝ ΑΡΤΗΡΙΑΚΩΝ ΑΝΤΙΣΤΑΣΕΩΝ ΔΡΑΣΤΙΚΟΥ ΑΡΤΗΡΙΑΚΟΥ ΟΓΚΟΥ ΑΙΜΑΤΟΣ ΕΚΚΡΙΣΗΣ ΒΑΖΟΠΡΕΣΣΙΝΗΣ ΔΡΑΣΤΗΡΙΟΤΗΤΑΣ ΣΥΜΠΑΘΗΤΙΚΟΥ ΔΡΑΣΤΗΡΙΟΤΗΤΑΣ ΣΡΑΑ ΚΑΤΑΚΡΑΤΗΣΗΣ ΝΑΤΡΙΟΥ ΥΔΑΤΟΣ

88 Primary Targets of Treatment in Heart Failure

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90 Neurohumoral activation
HEART FAILURE TREATMENT STRATEGIES Vasodilators Inotropics Symptom relief Diuretics Neurohumoral activation ACE-is, -blockers Spironolatone ARBs?, ANP? ET-1? Prevention of disease progression Gene therapy? Anti-remodeling strategies Reversal of HF Mann. Circulation 1999; 100:

91 Diuretics ACE inhibitors Beta Blockers Treatment Pharmacologic Therapy
HEART FAILURE Treatment Pharmacologic Therapy Diuretics ACE inhibitors Beta Blockers Digitalis Spironolactone Other Treatment of Heart Failure. Drugs This is a simple and pragmatic classification of the vast numbers and types of medications in the pharmacopoeia for the treatment of heart failure.

92 Stages in the Evolution
HEART FAILURE Treat risk factors Avoid toxics ACE-i in selected p. A Stages in the Evolution of Heart Failure Treatment B ACE-i  blockers In selected patients C ACE-i  blockers Diuretics / Digitalis a insuficiencia cardiaca es el resultado del fracaso del tratamiento de las cardiopatias (no hay insuficiencia cardiaca sin cardiopatia) Sin embargo, el diagnostico de insuficiencia cardiaca es elusivo, no solo por la dificltad de su definicion sino porque ademas es un espectro continuo que comienza eante la rpesencia de factores de riesgo de cardiaopatia e insuficiencia cardiaca D Palliative therapy Mech. Assist device Heart Transplant AHA / ACC HF guidelines 2001 4

93 ΔΙΟΥΡΗΤΙΚΑ ΚΑΙ ΚΑΡΔΙΑΚΗ ΑΝΕΠΑΡΚΕΙΑ
ΚΑΤΗΓΟΡΙΑ ΚΑΤΆ NYHA 1 2 3 4 ACE Inhibitors Diuretics plus different site action diuretic Edema β - blockers Digoxin AF Spironolactone

94 ΑΓΓΕΙΑΚΟ ΕΓΚΕΦΑΛΙΚΟ ΕΠΕΙΣΟΔΙΟ

95 Σήμερα το πρωί έγινε CT εγκεφάλου που δείχνει ένα ισχαιμικό έμφρακτο.
Άνδρας 73 ετών προσήλθε στα εξωτερικά ιατρεία με δεξιά ημιπάρεση και δυσφασία από 3ώρου. Σήμερα το πρωί έγινε CT εγκεφάλου που δείχνει ένα ισχαιμικό έμφρακτο. Τι αγωγή μας συμβουλεύετε να αρχίσουμε? Ηπαρίνη Ασπιρίνη Κλοπιδογρέλη Διπυριδαμόλη Ασπιρίνη+Κλοπιδογρέλη

96 Το Πρόβλημα AEE: αντιφατική και φτωχή αντιμετώπιση
Αλλά Tα AEE είναι μια ετερογενής ομάδα νευρολογικών συνδρόμων διαφόρου αιτιολογίας, διαφόρου παθοφυσιολογικού μηχανισμού, διαφόρου θεραπευτικής προσέγγισης (L. Caplan, Stroke: a clinical approach, 1993)

97 ΟΡΙΣΜΟΣ Aγγειακό Eγκεφαλικό Eπεισόδιο (AEE) είναι κάθε κλινικό σύνδρομο, ταχέως αναπτυσσόμενο, που οδηγεί σε εστιακή ή και γενική απώλεια της εγκεφαλικής λειτουργίας πάνω από 24 ώρες, αγγειακής και μόνο αιτιολογίας. J Clin Epidemiol, WHO MONICA project 1988

98 Παροδικού Ισχαιμικού ΑΕΕ Παροδικού Ισχαιμικού ΑΕΕ
Νέος ορισμός Παροδικού Ισχαιμικού ΑΕΕ (βασιζόμενος στο μη μόνιμη βλάβη του εγκεφαλικού ιστού) Παροδικό ισχαιμικό ΑΕΕ είναι ένα σύντομο επεισόδιο νευρολογικής δυσλειτουργίας προκαλούμενο από εστιακή εγκεφαλική ή αμφιβληστροειδική ισχαιμία, με κλινικά συμπτώματα διαρκείας <1 ώρας που αποδεδειγμένα (MRI) δεν οφείλονται σε οξύ εγκεφαλικό έμφρακτο. Παλαιός ορισμός Παροδικού Ισχαιμικού ΑΕΕ (βασιζόμενος στο χρόνο) Παροδικό ισχαιμικό ΑΕΕ είναι ένα αιφνίδιο νευρολογικό σύμπτωμα ή σημείο διαρκείας μέχρι <24 ωρών, αγγειακής αιτιολογίας, περιοριζόμενο σε μία περιοχή του εγκεφάλου ή του οφθαλμού και αρδευόμενο από συγκεκριμένη αρτηρία. N Engl J Med 2002;347:

99 Στοιχεία από τις ΗΠΑ Πρώτη αιτία μακρόχρονης σοβαρής αναπηρίας
500,000 νέα ΑΕΕ στις ΗΠΑ ετησίως 200,000 υποτροπές ΑΕE ετησίως Τρίτη αιτία θανάτων στις ΗΠΑ (167,400 θάνατοι το 1999) Ευθύνονται για > 50% όλων των νευρολογικών εισαγωγών στα νοσοκομεία Talking Points Stroke is the third leading cause of death in the United States, ranking behind cancer and heart disease, and is surpassed only by heart disease worldwide.(1,2) It accounts for about 10% of all deaths in most developed countries, including the United States.(3) About 30% of stroke victims die within 1 year; this percentage is higher among those over 65 years old.(1) The average hospital stay is 7.3 days for stroke victims in the United States.(4) Among stroke survivors in the Framingham Study:(5) - 31% required help in caring for themselves - 20% required help in walking - 71% had impairments that affected their ability to work in their previous capacity Background In 1948, the Framingham Heart Disease Epidemiology Study enrolled 5,209 residents of the Framingham, Massachusetts community—between the ages of 28 and 62—and followed up by examining them every 2 years since that time.(6) Framingham study data have been used to help establish stroke incidence, recurrence, and mortality rates, risk factors, and stroke-related morbidities. The severity of the stroke and the brain territory it affects determine the type and severity of residual disabilities, which may include speech difficulties, loss of sensory function, bilateral loss of motor control, or hemiparesis.(5) AHA, 2002 Heart and Stroke Statistical Update.

100 Stroke is the third leading cause of death worldwide
14 13 12 12 10 10 9 8 7 All deaths (%) 6 5 4 Reference Group 8 – Keep slide 2 Coronary Cancer Stroke Injury Respiratory HIV/AIDS heart disease tract infection HIV/AIDS = human immunodeficiency virus/acquired immune deficiency syndrome Reference: 1. World Health Organization. Global burden of stroke Available at:

101 Κύριες αιτίες θανάτου στην Ελλάδα-2005
Επιδημιολογικοί δείκτες Κύριες αιτίες θανάτου στην Ελλάδα-2005 (ανά πληθυσμού) ΣΝ Ca ΑΕΕ

102 Θνητότητα 28 ημερών από ΑΕΕ
κατά τα έτη 1994 και 2004 (CFR) 1994: 26.6% (95% CI, ) 2004: 25.5% (95% CI, ) % Vemmos et al, Stroke 1999, and ESC May 2005

103 Σύγχρονη κατάταξη ΑΕΕ Αιτιοπαθογενετικός μηχανισμός
Σύγχρονη κατάταξη ΑΕΕ Αιτιοπαθογενετικός μηχανισμός Όλες οι μελέτεs Αθήνας Ισχαιμικά % Αθηροσκληρωτική νόσος μεγάλων αγγείων 14-35% % Αιμοδυναμικό έμφρακτο (low-flow) Εμβολικό έμφρακτο (artery to artery) Κενοτοπιώδη έμφρακτα (Lacunes) % % Kαρδιοεμβολικά % % Κρυπτογενή (έμφρακτα αναπόδεικτης αιτίας) 12-37% % Σπάνια αίτια % % Αιμορραγίες % Ενδοεγκεφαλική % 15% Υπαραχνοειδής %

104 One year survival in patients with first-ever stroke “The Arcadia Stroke Registry”
Κενοτοπιώδη Αθηροσκληρωτικά Καρδιοεμβολικά Αιμορραγίες Vemmos et al, J Neurol Neurosurg Psychiatry 2000;69:

105 Νοσηλεία - Διαγνωστική προσπέλαση
ΕΠΕΙΓΟΝ CT κφ ή Ισχαιμικό έμφρακτο 2o CT scan 5-7 ημέρα Κφ στέλεχος US/αγγείων τραχήλου <50% >50% MRI US/καρδιάς Διαθωρακικό Αγγειογραφία DSA / MRA / CTA κφ Holter καρδιακού ρυθμού κφ Έλεγχος θρομβοφιλίας US/καρδιάς Διοισοφάγειο κφ

106 European Stroke Initiative 2003
Θεραπεία οξείας φάσης Γενικοί στόχοι (Acute stroke = medical emergency) Όλοι οι ασθενείς με οξύ ΑΕΕ πρέπει σήμερα να θεωρούνται επείγοντα περιστατικά Εκτίμηση και έναρξη θεραπείας <3 ώρες Εισαγωγή σε μονάδες ΑΕΕ ή “stroke team” European Stroke Initiative 2003

107 Nοσηλεία σε ειδικές μονάδες
Μονάδα Οξέων ΑΕΕ Nοσηλεία σε ειδικές μονάδες (Grade A) Μείωση θνητότητας 18-28% Μείωση θνητότητας + βαρειάς ανικανότητας 29% Stroke Unit Trialists’ Collaboration BMJ 1997;314:1151

108 Πρώτες ενέργειες στο θάλαμο 5-8 min
Θεραπεία οξείας φάσης Πρώτες ενέργειες στο θάλαμο 5-8 min Ζωτικά σημεία ΑΠ, σφύξεις, αναπνοή, θερμοκρασία Κλινική εξέταση Καρδιοαναπνευστική, αγγεία, νευρολογική Eνδοφλέβια γραμμή Normal, Ringers, λήψη αίματος Πρωτόκολλο Θρομβόλυσης

109 Γενική υποστηρικτική αγωγή Ι
Θεραπεία οξείας φάσης Γενική υποστηρικτική αγωγή Ι ΙV Normal saline cc/24h Αποφυγή dextrose, υπότονων διαλυμάτων Διατροφή (πνευμονία από εισρόφηση, 2η εβδομάδα) Δοκιμασία ύδατος, βιντεο-φλουοροσκόπηση με βάριο Ρινογαστρικός σωλήνας, γαστροστομία (>1 μήνα) Food Trial (Lancet. 2005) Γαστροστομία αυξάνει τη θνητότητα vs Levin Καμία διαφορά: πρώιμη διατροφή με Levin vs καθυστερημένης Θεραπεία καρδιακών αρρυθμιών, ισχαιμίας Πρόληψη φλεβοθρόμβωσης (κατάκοιτοι, ημιπληγικοί) Ελαστικές κάλτσες ISC LMWH σε δόσεις πρόληψης ασπιρίνη

110 Πρόληψη θρομβωτικών συμβαμάτων σε ασθενείς με ισχαιμικό ΑΕΕ
p = Φλεβοθρόμβωση δεξιού κάτω άκρου 18.1 UFH Ux2/24h Enoxaparin 40 mg sc/24h 10.2 p = Incidence (%) 9.6 4.5 p = 0.096 p = 0.059 1.0 0.9 0.3 0.2 VTE Proximal DVT Symptomatic VTE PE

111 Θεραπεία οξείας φάσης Θεραπείες μόνο σε κλινικές μελέτες (δεν έχει αποδειχθεί όφελος, δεν συνιστώνται) ΟΧΙ Νευροπροστατευτικά (grade A) Επείγουσα ενδαρτηρεκτομή (grade C) Επείγουσα αγγειοπλαστική (grade C) ΟΧΙ Αιμοδιύλιση (grade A) American Stroke Association Stroke. 2005;36: European Stroke Initiative Cerebrovasc Dis 2003;16:311–337

112 Γενική υποστηρικτική αγωγή ΙΙ Θεραπεία επιπλοκών
Θεραπεία οξείας φάσης Γενική υποστηρικτική αγωγή ΙΙ Θεραπεία επιπλοκών Υποξαιμία Χορήγηση Ο2 δεν χρειάζονται όλοι οι ασθενείς (grade B) Χορήγηση Ο2 σε κορεσμό <92% Διασωλήνωση: Ο2<50% ή CO2>50% ή αναπνοές >40 Υπόταση Χορήγηση υγρών Epinephrine 0.1–2 mg/h plus dobutamine 5–50 mg/h Υπεργλυκαιμία Θεραπεία >110 mg/dL Ινσουλίνη Θεραπεία λοιμώξεων Αντιβιοτικά Πυρετός Παρακεταμόλη (4-6 gr/24h)

113 Γενική υποστηρικτική αγωγή ΙΙΙ Θεραπεία επιπλοκών-υπέρταση
Θεραπεία οξείας φάσης Γενική υποστηρικτική αγωγή ΙΙΙ Θεραπεία επιπλοκών-υπέρταση Ασθενείς που δεν θα πάρουν θρομβόλυση Εάν: ΣΑΠ ≤220 ή ΔΑΠ ≤120 mmHg (2 μετρήσεις σε διάστημα 5 min) Μη θεραπεία Θεραπεία: οξύ έμφραγμα, οξύ πνευμονικό οίδημα, διαχωριστικό ανεύρυσμα Αντιμετώπιση: πόνου, κατακράτησης ούρων, κεφαλαλγία, διέγερση, κλπ Αντιμετώπιση επιπλοκών: υπογλυκαιμίας, υποξίας, εγκεφαλικού οιδήματος Εάν: ΣΑΠ ≥220 ή ΔΑΠ= ή ΜΑΠ >130 mmHg (ανά 20 min) ΙΜ κλονιδίνη mg ή και IV σε αραίωση ΙV νιτρογλυκερίνη 5 mg ή nitropaste IV εσμολόλη Εάν: ΔΑΠ > 140 mm Hg (2 μετρήσεις σε διάστημα 5 min) IV νιτροπρωσσικό νάτριο 0.5 mg/Kg/min Θρομβόλυση: ΣΑΠ > 185 mm Hg ή ΔΑΠ > 110 mm Hg ανάγκη θεραπείας

114 Γενική υποστηρικτική αγωγή ΙV Θεραπεία Οξειών Νευρολογικών Επιπλοκών
Θεραπεία οξείας φάσης Γενική υποστηρικτική αγωγή ΙV Θεραπεία Οξειών Νευρολογικών Επιπλοκών Εγκεφαλικό Οίδημα Κρανιεκτομή και αποσυμπίεση (Grade Α) Κορτικοειδή δεν συνιστώνται (Grade Α) Σε επιδείνωση ή αύξηση της ενδοκράνιας πίεσης IV Μαννιτόλη, Υπεραερισμός (Grade C) Παροχέτευση ΕΝΥ Επιληπτικές κρίσεις (4-5%) Θεραπεία όπως στις άλλες επιληπτικές κρίσεις American Stroke Association Stroke. 2005;36:

115 Θεραπεία οξείας φάσης Οδηγίες για θρομβόλυση σε οξύ ισχαιμικό ΑΕΕ σήμερα (ΑΗΑ Stroke Council) IV rt-PA 0.9mg/Kg, 10% bolus, 60min Χορήγηση φαρμάκου <3h ΙV στρεπτοκινάση δεν συνιστάται CT scan εκτίμηση από ειδικούς Κριτήρια αποκλεισμού NINDS Νοσηλεία σε ΜΕΘ ή Μονάδα οξέων ΑΕΕ Δυνατότητα αντιμετώπισης αιμορραγιών Circulation 1996;94: , Neurology 1999;53:S3-S14 (Grade A)

116 NINDS rt-PA Stroke Study rt-PA within 3 hrs after onset of symptoms
Θεραπεία οξείας φάσης NINDS rt-PA Stroke Study rt-PA within 3 hrs after onset of symptoms 30-50% favorable outcome vs % in placebo group Similar mortality rates Symptomatic Intracranial hemorrhage in 6.4% vs. 0.6% in placebo group The sooner the treatment is started the greater the benefit NEJM 1995;333:

117 1,796,513 admissions for ischemic stroke between 1999 and 2001
Thrombolysis for ischemic stroke in the United States: data from National Hospital Discharge Survey 1,796,513 admissions for ischemic stroke between 1999 and 2001 1,314 (0.07%) underwent intra-arterial thrombolysis 11,283 (0.6%) underwent intravenous thrombolysis διεθνώς <5% των ασθενών λαμβάνει rt-PA Qureshi AI, Neurosurgery 2005;57:647-54

118 Πρώιμη δευτερογενής πρόληψη Ασπιρίνη
Θεραπεία οξείας φάσης Πρώιμη δευτερογενής πρόληψη Ασπιρίνη Ασπιρίνη ( mg/24ωρο) εντός ωρών σε όλα τα ισχαιμικά. (grade A) Μπορεί επίσης να χορηγηθεί κλοπιδογρέλη ή συνδυασμός ασπιρίνης-διπυριδαμόλης. (grade A) Δεν χορηγείται αντί της θρομβολυτικής αγωγής (grade A) UFH ή LMWH ή κουμαρινικά δεν συνιστώνται Stroke 2006;37:

119 Δευτερογενής πρόληψη Καρδιοεμβολικά ΑΕΕ (Στην Οξεία φάση χορηγούμε μόνο ασπιρίνη, ακόμη και επί κολπικής μαρμαρυγής) Αρχίζουμε αντιπηκτική αγωγή, όταν το 2ο CT είναι (-) για αιμορραγικό έμφρακτο Μη βαλβιδική κολπική μαρμαρυγή Kουμαρινικά (ΙNR ) (Grade Α) Μηχανικές προσθετικές βαλβίδες Kουμαρινικά (ΙNR ) (Grade Α) Διατατική μυοκαρδιοπάθεια (Grade B) ? Kουμαρινικά (ΙNR ) Πρόσφατο έμφραγμα μυοκαρδίου ανεύρυσμα προσθίου τοιχώματος με ή χωρίς θρόμβο (Grade B) Kουμαρινικά για 3-6 μήνες (ΙNR ) Κουμαρινικά + ασπιρίνη ? Παλαιό έμφραγμα μυοκαρδίου Ασπιρίνη ( mg) (Grade A)

120 Συμπεράσματα (1) Το ΑΕΕ είναι ετερογενής ομάδα νευρολογικών συνδρόμων
Για να προτείνεις μια θεραπεία πρέπει να γνωρίζεις την ακριβή αιτία Η διαφορετική αιτιολογία εξηγεί την αποτυχία μεγάλων μελετών που συμπεριλαμβάνουν γενικώς όλα τα ισχαιμικά ΑΕΕ Υπάρχει ανάγκη μικρότερων μελετών που να αφορούν μόνο συγκεκριμένη αιτιολογία της νόσου πχ στένωση καρωτίδας

121 Συμπεράσματα (2) Το οξύ ΑΕΕ απαιτεί ταχεία μεταφορά του ασθενούς σε οργανωμένο κέντρο Η χορήγηση rt-PA βελτιώνει την αναπηρία των ασθενών όταν χορηγηθεί σε < 3 ώρες Η νοσηλεία και φροντίδα των ασθενών σε ειδικές μονάδες μειώνει τη θνητότητα και αναπηρία Η θεραπευτική παρέμβαση εξατομικεύεται για τον κάθε ασθενή Υπάρχει ανάγκη ενημέρωσης και συμμόρφωσης των γιατρών για τις αποδεδειγμένες θεραπευτικές παρεμβάσεις στην οξεία φάση των ΑΕΕ

122 ΕΥΧΑΡΙΣΤΩ