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Sumario Vol. 42 - Nº 3 Julio - Septiembre 2013

Acute Coronary Syndrome with Infective Endocarditis

Eliezer San Román García, Luis Miguel Morales Pérez,
Reinel Álvarez Plasencia

Instituto Nacional de Cardiología y Cirugía Cardiovascular.
Departamento de Terapia Intensiva Cardioquirúrgica.
Calle 17 Nº 702. El Vedado (10400) La Habana, Cuba.
E mail

Recibido el 29-ABR-13 – ACEPTADO después de revisión el 20-JUNIO-2013.
The authors declare not having conflicts of interest.
Rev Fed Arg Cardiol. 2013; 42(3): 222-223


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Acute coronary syndromes (ACS) are a frequent cause for going to the Emergency Service, an infrequent and severe complication in patients with the diagnosis of infective endocarditis (IE) [1], with an incidence difficult to estimate and high mortality. Its etiology is multifactorial. Sometimes, it is a finding in necropsies, with coronary arteries with no angiographically significant atherosclerotic lesions. The modality of presentation and the clinical evolution is similar to that observed in patients with atherotrombotic CAD [1].

Septic coronary embolism is mentioned as a frequent cause for ACS in these patients [2], with concomitant embolism in other territories, such as the spleen and the kidney [3]. Among other causes, external compression of the coronary arteries secondary to periannular complications (abscesses and pseudo-aneurysms) and severe acute aortic valve insufficiency stand out. The latter can cause per se, myocardial ischemia by decrease in coronary perfusion pressure and reduction of coronary flow reserve [4]. Also, the increase in the myocardial demand of oxygen by a fever syndrome, anemia and/or sepsis, mainly in patients in whom coronary arteriosclerotic lesions [5] coexist, may be responsible for ACS during the active infection of the disease. Another less frequent mechanism of myocardial ischemia over the evolution of IE, is coronary ostium obstruction by a vegetation[2]. This instance is more frequent in people ill with aortic valve infection and no microorganism is particular to this scenario [6].

The case of a 54-year-old man is presented. He had history of hypertension and rheumatic fever that presented a prolonged fever syndrome, ≥3 weeks. Between the supplementary diagnostic tests made, transesophageal echo was conducted, which documented endocarditis in native mitral and aortic valves, with negative hemoculture. The echocardiographic study showed pseudo-aneurysm in the mitral valve and at the level of the left coronary aortic valve, a large vegetation that was protruding in the left ventricular outflow tract (LVOT) and involved the left coronary ostium (Figure 1). The damaged aortic valve showed severe insufficiency that extended almost to the LV apex (Figure 2). In the evolution of the clinical symptoms of his IE, the patient presented ST elevation acute coronary syndrome (STEACS) in the anterior side (Figure 3). ACS was complicated by acute heart failure and cardiogenic shock. Before this extremely severe scenario, an emergency surgical management was followed without previous coronary angiography, a contraindicated procedure by the presence of aortic periannular abscessdocumented by echo. A double mitral-aortic valve replacement by a mechanic prosthesis was made. The post-operative period was very troublesome, complicated by acute renal failure, respiratory distress and cardiogenic shock refractory to the treatment. The patient died in multiorgan failure.

Figure 1. Transesophageal echo (TEE) that shows a vegetation at the level of the left coronary leaflet of the aortic valve.

 

Figure 2. Transesophageal echo (TEE) that allows verifying a vegetation at the level of the left coronary leaflet of the aortic valve, and severe aortic valve insufficiency.

 

Figure 3.Electrocardiographic tracing that shows extensive anterior myocardial infarction.

 

The anatomopathological study, when evaluating the arterial tree, did not find obstructive coronary lesions.

It was then interpreted in this clinical case, that the cause of the acute coronary event over the evolution of infective endocarditis in the native mitral and aortic valves, was the obstructive mechanism of the vegetation in the left coronary ostium, with the hemodynamic failure resulting from severe aortic failure.

 

 

REFERENCES

  1. Herzog CA, Henry TD, Zimmer SD. Bacterial endocarditis presenting as acute myocardial infarction: A cautionary note for the era of reperfusion. Am J Med 1991; 90: 392-7
  2. Tiurin VP, Korneev NV. The mechanisms of the development and diagnosis of myocardial infarct in septic endocarditis. Ter Arkh 1992; 64: 55-8.
  3. Sanz Ruiz R, San Román JA, Robles Alonso J, et al. Acute myocardial infarction secondary to left atrial mural endocarditis. Echocardiography 2005; 22: 621-2.
  4. Otto CM. Aortic regurgitation. En: Otto CM, editor. Valvular Heart Disease. 2.ª ed. Philadelphia: WB Saunders; 2004. p. 302-35.
  5. Ortega-Carnicer J, Ruiz-Lorenzo F, Benedicto A. Thrombolytic therapy for acute myocardial infarction in unsuspected infective endocarditis. Int J Cardiol 2005; 103: 108-10.
  6. Perera R, Noack S. Acute myocardial infarction due to septic coronary embolism. N Engl J Med 2000; 342: 977-8.

 

Publication: September 2013

 
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