Complications of Acute Myocardial Infarction —Diagnosis and Treatment—

JMAJ 45(4): 149–154, 2002

Hiroshi NONOGI

Director, Division of Cardiology and Emergency Medicine, National Cardiovascular Center

Abstract: For the past 20 years, the in-hospital mortality rate of acute myocardial infarction has signiﬁcantly decreased to less than 10%. This reduction can be attributed mainly to the development of acute-phase treatment such as reperfusion therapy. However, cardiogenic shock and cardiac rupture dominate more than 70% of the causes of death. CCUs have made efforts to treat these problems whose mortality rate is still high. For cardiogenic shock, maintenance of circulation fol- lowed by reperfusion therapy is necessary before it causes irreversible impairment of organ function. For cardiac rupture, a critical care system should be established to implement emergency surgical intervention following the early detection of cardiac tamponade, in addition to the emphasis on prevention in high-risk populations for cardiac rupture. Key words: Acute myocardial infarction; Cardiogenic shock; Cardiac rupture; Mortality; Complication

Introduction attributed to the progress of treatment of complications of acute myocardial infarction. Pump The mortality rate of acute myocardial infarc- failure and cardiac rupture (including ventric- tion in our CCUs has decreased from 12% in ular septal rupture) dominate approximately the early period (before the era of reperfusion 70% of the causes of death in the acute period. therapy, 1977–1986), through 8% in the middle Prognosis has been improved, but the mortality period (thrombolytic treatment widely adopted, rate is still high. Therefore, CCUs are making 1987–1992), to 5% in the late period [PTCA efforts to improve treatment effectiveness.1) (percutaneous transluminal coronary angio- The diagnosis and treatments against the two plasty) adopted as the main reperfusion ther- main causes of death will be discussed along apy, 1993–1998]. The improved prognosis can be with the major complications in the acute period

This article is a revised English version of a paper originally published in the Journal of the Japan Medical Association (Vol. 125, No. 5, 2001, pages 683–687).

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(%) Pump failure 100 Cardiac rupture 86 89 Ventricular septal 80 rupture 73 Table 1 Major Complications of Acute Myocardial Infarction

60 1. Pump failure (cardiogenic shock, heart failure) 2. Cardiac rupture (free wall rupture, ventricular septal rupture, papillary muscle rupture) 40 3. Arrhythmia Causes of death 4. Post-infarction angina 20 5. Right ventricular infarction 6. Pericarditis 0 7. Left ventricular thrombus and complicated embolism 1977ϳ86 1987ϳ92 1993ϳ98 (year) Mortality rate 12% 8% 5%

Fig. 1 Serial changes of causes of death in acute myocardial infarction (National Cardiovascular Center)

Table 2 Severity Classiﬁcation of Acute Myocardial Infarction (Killip Classiﬁcation)

Killip class Mortality rate in the original article Type I : no sign of CHF 6% (no rales in lung) Type II : pulmonary congestion limited to basal lung segments 17% (bi basilar rales) Type III: acute pulmonary edema 38% (rales in more than 50% of lung) Type IV: cardiogenic shock 81% CHF: congestive heart failure

listed in Table 1. rate would not improve without reperfusion even when using assisted circulation such as Evaluation of the Severity IABP (intra-aortic balloon pumping).

2) The classic Killip classification, one of the Cardiogenic Shock available methods for evaluating the severity of acute myocardial infarction, is still helpful for 1. Definitions (Table 3) the estimation of prognosis. As shown in Table Pump failure is defined as the condition in 2, the severity can be easily judged from physi- which cardiac output is insufficient to perfuse cal findings according to the Killip classifica- various body organs because of acute left ven- tion. Killip et al. reported that the mortality tricular contractile dysfunction caused by myo- rate increased with the rise of the type of the cardial infarction. Cardiogenic shock is defined disease, and that mortality rate in class IV (car- as myocardiogenic shock, except for when it is diogenic shock) was as high as 81%. In our caused by underlying diseases before the onset facility, the mortality rate was the same as that of infarction, mechanical complications, and of Killip-class IV before the era of reperfusion arrhythmia. Shock includes not only a low arte- therapy (Fig. 2), suggesting that the mortality rial blood pressure, but also severe, prolonged

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（%） Table 3 Deﬁnitions of Cardiogenic Shock 100 1. Systolic pressure: less than 90 mmHg 1977ϳ86 year 82 2. Existence of tissue hypoperfusion ϳ 80 1987 92 year (1) oliguria (less than 20 ml/h) ϳ 1993 98 year (2) mental obtundation (3) peripheral vessel contraction (cool, clammy skin, ＊ pϽ0.05 vs 1977ϳ86 ＊＊ 60 cyanosis) ＊＊ pϽ0.01 55

＊＊ Exceptions: hypotension accompanying conditions such as

Mortality 40 chest pain, hypotension of parasympathetic 40 nerves (bradycardia-hypotension syndrome: Bezold-Jarisch reﬂex), arrhythmia, drug abuse, 22 hypovolemia (e.g. dehydration and long-term administration of diuretics). 20 15 15 12 9 11 ＊ 442 0 Killip-I Killip-II Killip-III Killip-IV (2,361 cases)(439 cases) (216 cases) (183 cases) Medications From the emergency room catecholamine to the catheterization room Fig. 2 Serial changes of the mortality rate of acute myocardial infarction (National Cardiovascular Center)

Respiratory control Successful reperfusion IABP, PCPS Thrombolysis, PTCA tissue hypoperfusion.3) Coronary artery bypass surgery Heart 2. Treatment strategies4) Left ventricular assist device transplantation Because impairment of organ function caused Fig. 3 Medical guidelines for cardiogenic shock in acute by shock rapidly develops and becomes irre- myocardial infarction support versible within a short period, the most suitable IABP: intra-aortic balloon pumping, PCPS: percutaneous cardiopulmonary system, PTCA: percutaneous transluminal treatment should be adopted as early as possible. coronary angioplasty. Prolonged tissue hypoperfusion makes prognosis worse, leading to death from multiple organ failure even if hemodynamics is improved. Imme- diately after admission, respiratory control therapy or heparinization. If systolic pressure should be implemented for signiﬁcant hypox- does not rise to more than 80 mmHg within 15 emia with the administration of catecholamines. minutes, assisted device should be implemented. If 5–20␮g/kg/min of dopamine cannot achieve Treatment requiring a combination of reper- pressor effects, 5–20␮g/kg/min of dobutamine fusion therapy and maintenance of peripheral (DOB), or 0.05–0.2␮g/kg/min of noradrena- circulation is continued while in transit from line (NAd) should be administered. the emergency room (or CCU) to the catheteri- At the same time, the femoral artery and zation room. The reperfusion method of choice vein should be secured with a 5 Fr sheath to is PTCA. Prolonged shock with unavailability enable use of assisted device at any time. Punc- of a catheterization room should be treated turing is often difﬁcult if the femoral artery is with intravenous thrombolysis. not palpable. In principle, the internal jugular or subclavian vein should not be punctured in 3. Assisted devices case of shock. The reason is that there are cases (1) Intra-aortic balloon pumping (IABP): in which even one or two mispunctures can The results of IABP treatment without reper- lead to fatal bleeding because of thrombolytic fusion therapy for cardiogenic shock in acute

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Right atrium Artiﬁcal lung heat exchanger Inferior vena cava

Cannula for drawing blood Aorta

Cannula for blood Injection of blood

Arterial side

Drawing of blood Pump Venous side

Fig. 4 Percutaneous artiﬁcial cardiopulmonary system (PCPS) In case of a shock, 5 Fr sheath is inserted into femoral artery and vein to prepare for the initiation of PCPS. Priming (circuit ﬁlling) is completed within 5 minutes. Routine training is required.

myocardial infarction have not been encourag- with a circuit organized in sanitary conditions. ing. However, IABP is still an indispensable In order to enable a few night staff members to assisted device method when combined with deal with it, every nurse has routine training to reperfusion therapy. If systolic pressure is less complete circuit filling within 5 minutes as a part than 80 mmHg, and cardiac index is less than of lessons on cardio-pulmonary resuscitation. 2.2 l/min/m2 even with catecholamines, IABP If these types of assisted circulation and should be used. IABP serves as a pressure- reperfusion are insufficient, the use of a left support device, supporting only 15% of cardiac ventricular assist device to take care of part of output. Therefore, if cardiac output by own the cardiac pumping function should be consid- beat cannot be expected, the following PCPS ered. Because reduced cardiac function will be should be used. prolonged even after successful reperfusion, (2) Percutaneous cardiopulmonary support assisted circulation should be continued. Inten- system (PCPS):PCPS is a method in which sive care is required to maintain assisted circu- an artificial cardiopulmonary device enabling lation for a long period, and to prevent compli- assisted circulation can be made available by cations such as infection, bleeding, and lower inserting a cannula percutaneously. Perfusion limb ischemia. is maintained by delivering oxygen to venous blood derived from right atrium by means of 4. Efficacy of treatments for Cardiogenic an artificial lung, and by delivering the blood shock retrogradually into the femoral artery (Fig. 4). In cardiogenic shock, tissue hypoperfusion and It is possible to deliver blood at 2–4 l/min. If sys- acute myocardial infarction should be treated tolic pressure is less than 50mmHg, or repeated at the same time. Failing in either treatment ventricular fibrillation or tachycardia requiring would be lethal. Reperfusion of occluded coro- cardioversion is observed, PCPS should be used, nary artery is essential to improve prognosis. rather than IABP. To support coronary perfu- Moreover, it is important to achieve reper- sion, it should be combined with IABP. fusion within a short period from the develop- Because PCPS should be implemented ment of shock. If reperfusion cannot be achieved, quickly, our CCU is always equipped with PCPS the mortality rate is as high as 80% even with

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assisted device (Fig. 2). If a major vessel caus- increase in the rehabilitation. Because patients ing occlusion is reperfused irrespective of the showing significant retention of pericardial effu- type of reperfusion therapy, the in-hospital sion in echocardiogram over time and patients mortality rate is less than 40%, suggesting the with rapidly thinning of the infarction wall are importance of successful reperfusion. highly susceptible to cardiac rupture, they are A guideline of the ACC/AHA (American carefully monitored and the rehabilitation pro- College of Cardiology/American Heart Asso- cess is delayed. ciation) strongly recommends the use of PTCA.5) An oozing type of rupture with gradual reten- If PTCA is not available, or if it takes over 30 tion of bloody pericardial effusion leading to minutes to start it, intravenous infusion of tis- cardiac tamponade can be diagnosed by echo- sue plasminogen activator (t-PA) should be per- cardiography before the patient goes into shock. formed. However, because the mortality rate of Cardiac tamponade can be treated by perform- cardiogenic shock is still high, new therapies ing a surgical repair after drainage of pericar- such as myocardial protection methods should dial cavity. A sudden rupture, which immedi- be reviewed in addition to reperfusion therapy. ately leads to electro-mechanical dissociation, is lethal. It is treated by PCPS immediately after Cardiac Rupture the rupture to secure general circulation before stepping up, but the prognosis for sudden rup- Cardiac rupture occurs through an area of ture is unfavorable. transmural neurosis and expansion in the acute phase of myocardial infarction. It is classified as 2. Ventricular septal perforation left ventricular free wall rupture, ventricular Like free wall rupture, the peak incidence of septal perforation or papillary muscle rupture, septal rupture appears to be within a week after depending on the site of the lesions. The inci- infarction. When a new, harsh, loud holosys- dence of rupture shows two peaks: within 24 tolic murmur is heard between the third and hours after the onset of infarction, and one the fourth intercostal of the left parasternum, week later. The mortality rate of free wall rup- ventricular septal perforation is strongly sus- ture is high. It is one of the concerns for CCUs pected. It can be diagnosed by confirming the in parallel with death from pump failure. The existence of a left-to-right interventricular shunt frequency is low, but it does have a noticeable using two-dimensional echocardiography, and incidence. The frequency of the oozing type has by confirming a significant increase in oxygen been increasing compared with the sudden saturation from the right atrium to pulmonary rupture type, which is lethal and requires pre- artery. The frequency of ventricular septal per- ventive measures. foration in our facility is approximately 1% of all myocardial infarction. Out of 33 patients, 18 1. Free wall rupture underwent an operation, and 12 of them sur- In cases of successful reperfusion, the second vived and were discharged from the hospital. peak of cardiac rupture is reported to decrease, Only 2 out of 15 patients who did not undergo while the possibility of increased cardiac rup- surgery survived and were discharged from the ture caused by thrombolytic therapy is pointed hospital. Therefore, the operation should be out. Therefore, for patients over the age of 70 performed whenever possible. Especially for complicated with hypertension, PTCA is often shock, early surgical intervention is essential. the reperfusion method used. Attention should be paid to suppress systolic 3. Papillary muscle rupture pressure under 120 mmHg in the acute phase Severe mitral regurgitation occurs after acute of myocardial infarction, and under 20 mmHg myocardial infarction in papillary muscle rup-

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ture, rapidly progressing to shock from left- tality of acute myocardial infarction. sided heart failure. As cardiac murmur associ- ated with mitral regurgitation is brief or even REFERENCE completely absent in patients with reduced car- 1) Nonogi, H.: Therapeutic strategies to improve diac function, echocardiography is an effective long-term prognosis in acute myocardial infarc- diagnostic tool. Because signiﬁcant mitral regur- tion. J Jpn Soc Intensive Care Med 1999; 6: gitation is an indication to perform early sur- 189–195. gical correction, valve replacement or repair 2) Killip, T. and Kimball, J.T.: Treatment of myo- should be performed. cardial infarction in a coronary care unit. A two year experience with 250 patients. Am J Cardiol 1967; 20: 457–464. Conclusion 3) Nonogi, H.: Deﬁnition and diagnostic standard of cardiogenic shock. ICU and CCU 2000; 24: The prognosis for acute myocardial infarc- 211–221. (in Japanese) tion after admission has improved for the past 4) Residents of National Cardiovascular Disease 20 years because of the progress in treatments Center Eds: CCU Manual. Chugai Igakusya, such as reperfusion therapy. However, as men- 2000. (in Japanese) tioned in the present paper, the mortality rate 5) Ryan, T.J., Antman, E.M., Brooks, N.H., et al.: of cardiogenic shock and cardiac rupture is still ACC/AHA guidelines for managements of high, and further efforts should be made to patients with acute myocardial infarction: Executive summary and recommendations: A improve treatment effectiveness. The mortality report of the American College of Cardiol- rate before admission is higher, and 30–50% is ogy/American Heart Association Task Force estimated to die outside the hospital. Establish- on Practice Guidelines (Committee on Man- ment of a cardiovascular critical care system is agement of Acute Myocardial Infarction). Cir- urgently required to reduce the general mor- culation 1999; 100: 1016–1030.

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