Acute Heart Failure After Myocardial Infarction

We compared two groups of patients after acute myocardial infarction. First group was treated with fi brinolytics and they were hospitalized within six hours from the beginning of the fi rst chest-symptoms, and second group that did not come within optimal time was treated with anticoagulants only. Th e patients were classifi ed according to Killip-classifi cation, shock-index and TIMI-risc-score after myocardial infarction. Results prove great benefi t of fi brinolytic therapy in optimal time, concerning both keeping myocardial muscle mass and myocardial


Introduction
Cardiac pump failure is the leading cause of circulatory failure and in-hospital death from acute MI (myocardial infarction).Manifestations of circulatory failure may include a weak pulse, low blood pressure, cool extremities, a third heart sound, pulmonary congestion, oliguria, and cold sweat perspiration.However, several distinct mechanisms, hemodynamic patterns, and clinical syndromes characterize the spectrum of circulatory failure in acute myocardial infarction.Each requires a specifi c approach to diagnosis, monitoring, and therapy.Th e degree of left ventricular dysfunction correlates well with the extent of acute ischemia/infarction.Hemodynamic compromise becomes evident when impairment involves  to  of the left ventricle, and cardiogenic shock or death occurs with involvement left ventricular muscle of  or more.Pulmonary congestion and S and S gallops are the most common physical fi ndings.Early recanalization (via thrombolytics, PCI, or CABG) is the most eff ective therapy to reduce infarct size, ventricular dysfunction, and associated heart failure.Medical treatment of heart failure related to the ventricular dysfunction of acute myocardial infarction is otherwise generally similar to that of heart failure in other setting and includes adequate oxygenation and diuresis (begun early, blood pressure permitting, and continued long-term if needed).Intravenous vasodilator therapy (for preload and after load reduction), inotropic support, and intra-aortic balloon counter pulsation are indicated in cardiogenic shock Nitrates (nitroglycerin) reduce preload and eff ectively relieve congestive symptoms (,).Left heart weakness is linked with both longand short-term poor prognosis.Clinical symptoms begin with dyspnea, sinus tachycardia, a third heart sound and murmurs which are fi rst detected on the pulmonary basis but then spread and involve whole lungs.However, developed pulmonary congestion is not necessarily followed by the auscultator signs.Clinical examination (heart sound auscultation and follow-up of the rest of the vital parameters) must be periodically (repeatedly) done in all patients in the early phase of infarction.General measures include follow-up of arrhythmia, control of the electrolyte level in serum as well as registration of the collateral conditions like valvular dysfunction or lung diseases.Pulmonary congestion can be detected by the x-ray examination.Echocardiography is a very useful method in the estimation of the extent of the infarction, valvular function and appearance of mechanical complication like mitral regurgitation and ventricular septal defect, conditions that might be responsible for heart function irregularity.In patients with serious heart failure and schock ,PCI or surgical revascularization can improve survival (, , ).Heart failure grade can be defi ned according to Killip classifi cation (Table ).TIMI -risc score (Th e Th rombolysis in Myocardial Infarction Study Group) has a higher prognostic value, especially in the estimation of one-and six-months survival (Table ) ().Relative or absolute hypovolemia is a frequent cause of hypotension and circulatory failure and is easily corrected if recognized and treated promptly.Poor hy-dration, vomiting, diuresis, and disease-or drug-induced peripheral vasodilation may contribute.Hypovolemia should be identified and corrected with intravenous fl uids before more aggressive therapies are considered.An empirical fl uid challenge may be tried in the appropriate clinical setting (e.g., hypotension in absence of congestion; inferior or RV infarction; hypervagotonia).If fi lling pressures are measured, cautious fl uid administration to a pulmonary capillary wedge pressure of up to about  mm Hg may optimize cardiac output and blood pressure without impairing oxygenation.() Right ventricular ischemia and infarction occur with proximal occlusion of the right coronary artery (before the take off of the right ventricular branches).Ten to fifteen percent of inferior acute ST-elevation myocardial infarctions show classic hemodynamic features, and these patients form the highest risk subgroup for morbidity and mortality ( to  versus < hospital mortality).Improvement in right ventricular function commonly occurs over time, suggesting reversal of ischemic stunning and other favorable accommodations, if short-term management is successful.Hypotension with clear lung fi elds and elevated jugular venous pressure in the setting of inferior or inferoposterior acute myocardial infarction should raise the suspicion of right ventricular infarction.Kussmaul's sign (distention of the jugular vein on inspiration) is relatively specifi c and sensitive in this setting.Right-sided ECG leads show ST-elevation, particularly in VR, in the fi rst  hours of RV infarction.Echocardiography is helpful in confirming the diagnosis (dilation of right ventricular and dysfunction are observed).If right heart pressures are measured, a right atrial pressure of ≥ mmHg and ≥ of the pulmonary capillary wedge pressure is relatively sensitive and specifi c for right ventricular ischemic dysfunction (,).Management of right ventricular infarction consists of early maintenance of right ventricular preload, reduction of right ventricular afterload, early recanalization, short-term inotropic support if needed, and avoidance of vasodilators (e.g.nitrates) and diuretics used for left ventricular failure (which may cause marked hypotension).Volume loading with normal saline alone is often eff ective.If the cardiac output fails to improve after , to  liter of fl uid, inotropic support with dobutamine is recommended.High-grade atrioventricular block is common, and restoration of atrioventricular synchrony with temporary atrioventricular sequential pacing may lead to substantial improvement in cardiac output.Th e onset of atrial fibrillation (in up to one third of right ventricular infarcts) may cause severe hemodynamic compromise requiring prompt cardioversion.Early coronary recanalization with thrombolysis or PCI markedly improves outcomes(,,).Cardiogenic shock is a form of severe left ventricular failure characterized by marked hypotension (systolic pressures less than  mm Hg) and reductions in cardiac index (<, L/min/ m) despite high left ventricular fi lling pressure (pulmonary capillary wedge pressure greater than  mm Hg).Th e cause is loss of a critical functional mass (>) of the left ventricle.Cardiogenic shock is associated with mortality rates of more than  to  despite aggressive medical therapy.Risk factors include age, large (usually anterior) acute myocardial infarction, previous myocardial infarction, and diabetes.In patients with suspected shock, hemodynamic monitoring and intra-aortic balloon counterpulsation (IABP) are indicated ().Intubation is often necessary.With early application, urgent mechanical revascularization (PCI or CABG) aff ords the best chance for survival, especially in patients younger than  years old ().Th e goal of risk stratifi cation before and early after discharge for acute myocardial infarction is to assess ventricular and clinical function, latent ischemia, and arrhythmic risk, and to use this information for patient education and prognostic assessment and to guide therapeutic strategies ().

CARDIAC CATHETETERIZATION AND NONIVANSIVE STRESS TESTING
Risk stratifi cation generally involves functional assessment by one of three strategies: cardiac catheterization, submaximal exercise stress ECG before discharge (at  to  days), or symptom-limited stress testing at  to  weeks after discharge ().Many patients with ST elevation-acute myocardial infarction undergo invasive evaluation for primary PCI or after thrombolytic therapy.Catheterization generally is performed during hospitalization for patients at high risk.In others, predischarge submaximal exercise testing (to peak heart rate of  to  beats/min or  of the predicted maximum) appears safe when performed in patients who are ambulating without symptoms; it should be avoided within  to  days of acute myocardial infarction and in patients with unstable post myocardial infarction angina, uncompensated heart failure, or serious cardiac arrhythmias.Alternatively or in addition, patients may undergo symptom-limited stress testing at  to  weeks before returning to work or other increased physical activities.Abnormal test results include not only ST-depression but also low functional capacity, exertional hypotension, and serious arrhythmias.Patients with positive tests are considered for coronary angiography ().Th e sensitivity of stress testing can be augmented with radionuclide perfusion imaging (thallium- and/or technetium-m-sestamibi; or echocardiography.Supplemental imaging also can quantify the left venticular ejection fraction and size the area of infarct and/or ischemia.For patients on digoxin with ST-segment changes that preclude accurate ECG interpretation (e.g., baseline LBBB or LV left ventricular hypertrophy), an imaging study is recommended with initial stress testing.In others, an imaging study may be performed selectively for those in whom the exercise ECG test is positive or equivocal.For patients unable to exercise, pharmacological stress testing can be performed using adenosine or dipyridamole scintigraphy or dobutamine echocardiography ().

Patients and Methods
Research included  patients with the myocardial infarction, with ST elevation diagnosed and treated on the Department of Internal Medicine of the General Hospital "Prim.Dr A. Nakaš", Sarajevo in the period st February .-stFebruary .Criteria for the entering the study group were: -age  - -fi rst myocardial infarction, -balanced sexual distribution due to better group homogenization.Criteria for the exclusion of patient from the study group were: -age below  and above  -former myocardial infarction (s), Study group had  patients ( male and  female) admitted to the unit of intensive care with developed symptoms of acute myocardial infarction: ST elevation within  hours (most of them within  hours) from the beginning of symptoms, all treated with fi brinolytics, anticoagulants and adjuvant therapy.Control group were  patients ( male and  female) admitted to the unit of intensive care with developed symptoms of acute myocardial infarction and ST elevation but with contraindication for fi brinolytics which therefore were not administrated.Most of the control group patients were admitted to the Hospital in the period longer than  hours from the beginning of the symptoms.We divided patients in groups according to Killip-classiffi cation and parameters of the clinical presentation of the disease in the moment of hospitalization (Table ., Graph .)In the fi rst day of hospitalization according to Killip-classiffication there is no statistically significant diff erence among the groups.According to TIMI -risk score there is a statistically signifi cant diff erence between the research and control group of patients (table., graph ).Patients that avoided fi brinolysis got additional  points according to TIMI -risk score that made the statistically signifi cant diff erence among the groups.Analyzing of the -day survival rate of the research and control group we notifi ed higher survival rate of the research group -, , compared to ,  rate of the control group (table .,graph .).Statistically, in the study group survived  (/) patients and in control group  (/) patients and the survival rate after  days is higher in the study group for  .Both groups were analyzed related to Killip classification done at the moment of patient's hospital admittion and correlation of the classifi cation results to the survival rate(table .,graph .).Division of patients into the Killip classes proved to be a good predictor of one -month survival after acute myocardial infarction -STEMI.

KILLIP CLASS ON THE PATIENT HOSPITAL ADMITTION AND LOCALIZATION OF THE AMI
Both groups were analyzed related to correlation between Killip-classification in the moment of the patient's admition and myocardial infarction localization (table .,graph .).

TIMI -RISK SCORE AND -DAYS SURVIVAL
Both groups were analyzed related to TIMI-risk-score and correlation of the risk-score to the -days survival rate(table .,graph .)

EF () ESTIMATION AT THE SURVIVED PATIENTS AFTER - DAYS FROM STEMI
Patients who survived divided in two groups (study and control) as defi ned in the study were analyzed.Th e aim of the analysis was to estimate whether groups of the survived patients showed signifi cant diff erence regard-ing estimated ejection fraction (EF) (Table ,Graph ).Study and control group of patients after - days showed signifi cant diff erence regarding estimated ejection fraction EF().In the study group, EF() was significantly higher.Percentage relation is: - , patients in the control group had EF over   -,  patients in the study group had EF over   which makes ,  higher incidence of survived EF() in the study group.Study group had slightly, statistically insignifi cant higher survival rate of the patients with heart failure and shockindex higher than  compared to the control group of patients (Table , Graph ) Comment: Groups are not statistically signifi cant.Cardiogenic shock mortality was  .

Discussion
During the research there were a certain variations of results related to sex and age parameters but with no statistical signifi cance.Th ere is also diff erence related to distribution of patients according to Killip-classifi cation which points the heart pump function.In the study group  patients were in Killip class I,  patients with Killip-class II-IV.In control group  patient was Killipclass I and  patients were Killip-class II-IV.Neither this parameter made significant statistical difference (Table , Graph ) TIMI risk -score describes risk -factors and hemodynamic parameters of the patients in the moment of hospital admittion in more details and proved to be useful predictor of the -days survival.
In study group there were  patients with TIMI score -; patients with TIMI-risk score - and  patients with score over .In control group there were  patients with TIMI score -; patients with TIMI score - and  patients with score over .Even absolute fi gures show that there is a signifi cant statistical diff erence between the groups (Table ,Graph ).Th is signifi cant statistical diff erence between the groups according to this score is result of the fact that in the very beginning patients who did not get fi brinolytics got adittional  points.One-month survival rate of both groups pointed out that in the study group there was a  survived patients after a month which makes ,  from the total of all patients; in the control group  patients e.g.,  of total number of patients survived.Both absolute and relative calculations point the statistically signifi cant higher number of survived patients in the study group.Mortality of the study group: / x  =   Mortality of the control group/ x  = ,  Mortality in the group that got the fibrinolytics was for   lower than in the control group which points the very favourising effect of fibrinolytic therapy.Study shows that fibrinolytic therapy had favourising effect on the -days survival of the patients with STEMI (Table ,Graph ).More benefits were proved at the patients with anterior localization of myocardial infarction where mortality reduction was  while results of our study proved the following: -in the study group the mortality of patients with anterior localization of the myocardial infarction was , , and in control group , .Th e survival in the study group was higher for , ; -in the study group the mortality of patients with inferior localization was  , and in control group , .Th e survival in the study group was higher for , .
Killip-class of patients (in the moment of the patient's hospital admittion ) as predictor of the -days survival was compared with the survival rates as a prognostic parameter (  ().Th e rest of the regularly perfused myocardium in the new situation tends to hypercontraction unless there is a consecutive coronary disease of it's irrigation area.Coronarography examination of the patients in this study showed that high percentage of them had multivascular heart disease which caused that incidence of the heart failure in the myocardial infarction was relatively high.More frequent heart failure at the younger population of patients can be explained with the insuffi tiently developed collateral circulation which could not supply the ischemic area.Th e worse form of the heart failure was low blood pressure appearance with the signs of the pulmonary congestion and peripheral hypoperfusion with refl ex tachycardia.Th is situation requires prompt differentiation of cardiogenic shock versus hypovolemia or consecutive right venticule infarction.Important parameter is CVP measurement but sometimes we are not in position to measure it although situation requires that.We should reconsider possibility of right ventricle myocardial infarction when we have infero-posterior localization of the infarction (than we have proximal occlusion of the right coronary artery), when pulsing overloaded neck venes are obvious and when we have signs of hepatal congestion (hepatojugular refl ux), with systemic hypotension , without pulmonary congestion.Analysis of the group of patients with the signs of the heart failure with the systolic pressure/puls index higher than  (where we registrated systolic pressure below  mm Hg with  or more beats per minute-tachicardia) and the signs of the peripheral hypoperfusion.
Th is analysis showed the following (Table , Graph ): -the study group had  patients with above mentioned hemodinamic parameters out of which  died ; -In control group there were  patients with  lethal outcomes.
Cardiogenic shock was highly lethal (almost  ) but similar results is registrated even in the best equipped health institutions where intraaortal balloon-pump could be placed and urgent coronarography and PTCA with stent could be done according to modern protocols.In our study mortality rate of the cardiogenic shock was .Th e only patient who survived had the consecutive infarction of the right ventricule which caused the above described hemodinamic parameters.He died  months after the fi rst infarction due to development of the heavy global decompensated ischaemic cardiomyopathy.Th e only patient in the control group who survived was a woman who was in hypovolemia due to profuse swettening and stabilized by the volume compensation.

Table  ,
Graph ).In the study group  of survived  patients had Killip-class I, and in control group  of  survived patients had Killip-class I at the hospital admittion.Killip-class I showed high statistically signifi cant positive correlation with -days survival rate.Comparation of the Killip-class at the hospital admittion and localization of the myocardial infarction showed the following (Table , Graph ) In the group with Killip-class I at the hospital admittion was approximately same number of those patients with anterior and inferior localization of myocardial infarction.Statistic analysis showed that both localization were equally presented in both groups of Killip-classifi cation.According to the fact that anteroseptal locatisation of myocardial infarction is usually more massive, it would be expected that this localization is presented with higher Killip-class, e.g. group II-IV, but we did not prove that.Possible explanation for such results could be that majority of patients who were later examined by coronarography had multivascular heart disease and were presented as fi rst myocardial infarction both anterior or inferior localization.Detailed analysis of the risk -factors and hemodynamic parameters at the moment of patient's hospital admittion is implemented in TIMI-risk -score for both group of patients.(table,graph ) A fact that all patients with TIMI risk -score less or equal to  survived, leads to the conclusion that TIMI-scor value less or equal to  well correlates to the one-month survival.If less than  of the heart muscle mass is aff ected by the lesion, signs of the left ventricule heart failure are to be expected