Association of hemostasis and inflammation biomarkers with outcomes in acute coronary syndromes.

Plaque rupture triggers a prothrombotic response that is counterbalanced by a fibrinolytic response. d -dimer serves as a marker of both processes. Inflammatory mediators are also released, evidenced with the rise of high-sensitive C reactive protein (hsCRP). Current evidence with these biomarkers has shown conflicting results. Determine an association between d -dimer and hsCRP within hospital and 1-year mortality in patients with acute coronary syndromes. In total, 127 patients were included. In-hospital mortality was 5.7%, and 1-year all-cause and cardiovascular mortality were 14.6 and 9.7%, respectively. The median of admission d -dimer for patients who died during hospital stay was higher than those who survived [4.59 (interquartile ranges (IQR) 1.94-6.05 µg/ml fibrinogen equivalent units (FEU)) vs. 0.56 (IQR 0.31-1.12 µg/ml FEU), P  = 0.001]. At 1-year follow-up, the median of admission d -dimer for patients who died was significantly higher than those who survived: 1.55 (IQR 0.91-5.08 µg/ml FEU) vs. 0.53 (IQR 0.29-0.90 µg/ml FEU), P  < 0.001. Positive d -dimer vs. negative d -dimer at admission analysis evidenced that almost 25% of the positive patients were dead at 1-year follow-up (22.4 vs. 2.4% negative d -dimer, P  = 0.011). Multivariate logistic regression analysis showed that d -dimer has an independent association with 1-year mortality [odds ratio 1.06 (95% confidence interval 1.02-1.10), P  = 0.006]. Positive significative correlations between d -dimer and hsCRP levels ( R  = 0.56, P  < 0.001) were found. High levels of admission d -dimer were strongly associated with in-hospital and 1-year mortality. Significant correlations with hsCRP could explain the inflammatory nature that led to poorer outcomes. d -dimer could be useful in risk stratification in acute coronary syndromes; however, a specific threshold should be defined for this type of patient.

Neurohumoral response and stress hyperglycemia in myocardial infarction.

Background: Hyperglycemia is associated with an increased risk for death in acute coronary syndromes. This could be related to underlying glucose metabolism abnormalities or be caused by a counter-regulatory stress response. However, there is a paucity of data on the relationship between stress hormones, hyperglycemia, and clinical outcomes in myocardial infarction. Methods: Single-center, prospective, observational study. Patients admitted to the coronary care unit with a diagnosis of myocardial infarction were included. On admission, blood samples were obtained to measure serum glucose, cortisol, and catecholamines. A second sample was obtained at 8 AM after 48 h from admission. Results: There was a mild and positive correlation between serum cortisol and glucose (Spearman's rho = 0.24, p = 0.005), and no significant correlation was found between glucose and catecholamines. A similar correlation between cortisol and glucose among diabetics and non-diabetics was observed. Significantly higher serum cortisol and glucose levels were present in patients who developed heart failure or died during hospitalization. The association between glycemia and mortality lost significance in multivariate analysis, with a significant interaction term with cortisol (p = 0.003). Conclusion: Cortisol is a key responsible for stress hyperglycemia, and its deleterious effects on the cardiovascular system could be the cause for worst outcomes associated with hyperglycemia in ACS. Further research is warranted to ascertain this relationship and to investigate potential therapeutic targets.

Cortisol-Mediated Stress Response and Mortality in Acute Coronary Syndrome.

Acute coronary syndrome is a frequent cause of morbidity and mortality, and a known stress response trigger. We aim to investigate the association between cortisol, as a primary stress hormone, and prognosis/mortality in this scenario. Single-center, prospective, observational, and analytical study in patients admitted for acute coronary syndrome. Clinical characteristics and prognosis markers were registered, along with serum cortisol levels on admission and in-hospital mortality. Cortisol levels were higher in patients with a depressed ST segment (18.22 ± 13.38 µg/dL), compared to those with an isoelectric ST segment (12.66 ± 10.47 µg/dL), and highest in patients with an elevated ST segment (22.61 ± 14.45 µg/dL), with P< 0.001. Also, cortisol was significantly increased in patients with elevated troponin I values (18.90 ± 14.19 µg/dL vs 11.87 ± 8.21 µg/dL, P< 0.001). Patients with Killip-Kimball class I or II had a lower mean serum cortisol (14.66 ± 10.82 µg/dL) than those with class III or IV (41.34 ± 15.57 µg/dL), P< 0.001. Finally, we found that patients who died during hospitalization had higher cortisol on admission: 36.39 ± 17.85 µg/dL vs 15.26 ± 11.59 µg/dL, P= 0.003. Cortisol was directly related to the electrocardiographic presentation of ACS and with the maximum troponin I value. This indicates that serum cortisol levels parallel the extension of ischemia and myocardial injury, and in this way affect the clinical prognosis, evidenced by the Killip-Kimball class and the increase in mortality.

[MINOCA, infarction with normal coronaries. The fall of the paradigm ?] / MINOCA, infarto con coronarias normales ¿ la caída del paradigma ?

Myocardial infarction is the leading cause of death in the world, being the coronary atherosclerotic obstruction the main finding. Although 6% of all the patients had no significant coronary arteries disease on coronary angiography, defined by lumen vascular obstruction greater than 50%. This type of cases was defined by the term MINOCA (myocardial infarction with non-obstructive coronary arteries). They are usually young women, with cardiovascular risk factors, high cardiac biomarkers with non-ST elevation in the electrocardiogram. The main etiologies are myocarditis, Takotsubo syndrome and subendocardial myocardial infarction. We present the case of a 65 years-old woman with history of hypertension and complete left bundle branch block, who was admitted to the emergency department with typical chest pain, complete left bundle branch block in the electrocardiogram, with negative Sgarbossa criteria and positive cardiac biomarkers. The echocardiography evidenced inferolateral regional wall motion abnormalities, and the coronary angiography a single non-significative lesion (40%) in the proximal segment of the circumflex artery. Cardiac magnetic resonance evidenced subendocardial late adolinium enhancement in inferolateral medial with latero-apical extension segments consistent with circumflex artery-related infarction. This case illustrates an example of MINOCA secondary to myocardial infarction with posterior spontaneous thrombolysis, in which the clinical presentation was typical, however the coronary angiography showed non obstructive lesions. Therefore, another complementary imaging methods were needed such as the cardiac magnetic resonance.

El infarto agudo de miocardio es la principal causa de muerte en el mundo, siendo la obstrucción coronaria aterosclerótica el hallazgo más frecuente. Sin embargo, el 6% de los pacientes no presenta lesiones angiográficamente significativas, definidas por obstrucción de la luz vascular mayor al 50%. Estos casos se han definido bajo el término MINOCA (myocardial infarction with non-obstructive coronary arteries). Suelen ocurrir en mujeres jóvenes, con factores de riesgo cardiovascular, elevación de biomarcadores cardíacos e infradesnivel del segmento ST en el electrocardiograma. Las principales etiologías son la miocarditis, el síndrome de Takotsubo y el infarto subendocárdico. Presentamos el caso de una mujer de 65 años con antecedentes de hipertensión arterial y bloqueo completo de rama izquierda previo, que ingresó con ángor, imagen de bloqueo completo de rama izquierda en el electrocardiograma con criterios de Sgarbossa negativos y biomarcadores cardíacos positivos. En el ecocardiograma evidenció trastorno en la motilidad de la pared inferolateral y en la coronariografía solo una lesión no significativa (40%) en segmento proximal de la arteria circunfleja. La cardiorresonancia, en la secuencia de realce tardío de gadolinio, mostró retención de contraste subendocárdico a nivel de los segmentos inferolateral medial con extensión lateroapical compatible con infarto correspondiente a territorio de arteria circunfleja. Este caso ilustra un ejemplo de MINOCA secundario a infarto subendocárdico con trombólisis espontánea, en el que la presentación clínica fue típica, sin embargo en la coronariografía no se observaron lesiones significativas, por lo que fue necesario complementar con otro método de imágenes: la cardiorresonancia.

Minoca, infarto con coronarias normales ¿La caída del paradigma? / MINOCA, infarction with normal coronaries. The fall of the paradigm ?

El infarto agudo de miocardio es la principal causa de muerte en el mundo, siendo la obstrucción coronaria aterosclerótica el hallazgo más frecuente. Sin embargo, el 6% de los pacientes no presenta lesiones angiográficamente significativas, definidas por obstrucción de la luz vascular mayor al 50%. Estos casos se han definido bajo el término MINOCA (myocardial infarction with non-obstructive coronary arteries). Suelen ocurrir en mujeres jóvenes, con factores de riesgo cardiovascular, elevación de biomarcadores cardíacos e infradesnivel del segmento ST en el electrocardiograma. Las principales etiologías son la miocarditis, el síndrome de Takotsubo y el infarto subendocárdico. Presentamos el caso de una mujer de 65 años con antecedentes de hipertensión arterial y bloqueo completo de rama izquierda previo, que ingresó con ángor, imagen de bloqueo completo de rama izquierda en el electrocardiograma con criterios de Sgarbossa negativos y biomarcadores cardíacos positivos. En el ecocardiograma evidenció trastorno en la motilidad de la pared inferolateral y en la coronariografía solo una lesión no significativa (40%) en segmento proximal de la arteria circunfleja. La cardiorresonancia, en la secuencia de realce tardío de gadolinio, mostró retención de contraste subendocárdico a nivel de los segmentos inferolateral medial con extensión lateroapical compatible con infarto correspondiente a territorio de arteria circunfleja. Este caso ilustra un ejemplo de MINOCA secundario a infarto subendocárdico con trombólisis espontánea, en el que la presentación clínica fue típica, sin embargo en la coronariografía no se observaron lesiones significativas, por lo que fue necesario complementar con otro método de imágenes: la cardiorresonancia.

Myocardial infarction is the leading cause of death in the world, being the coronary atherosclerotic obstruction the main finding. Although 6% of all the patients had no significant coronary arteries disease on coronary angiography, defined by lumen vascular obstruction greater than 50%. This type of cases was defined by the term MINOCA (myocardial infarction with non-obstructive coronary arteries). They are usually young women, with cardiovascular risk factors, high cardiac biomarkers with non-ST elevation in the electrocardiogram. The main etiologies are myocarditis, Takotsubo syndrome and subendocardial myocardial infarction. We present the case of a 65 years-old woman with history of hypertension and complete left bundle branch block, who was admitted to the emergency department with typical chest pain, complete left bundle branch block in the electrocardiogram, with negative Sgarbossa criteria and positive cardiac biomarkers. The echocardiography evidenced inferolateral regional wall motion abnormalities, and the coronary angiography a single non-significative lesion (40%) in the proximal segment of the circumflex artery. Cardiac magnetic resonance evidenced subendocardial late gadolinium enhancement in inferolateral medial with latero-apical extension segments consistent with circumflex artery-related infarction. This case illustrates an example of MINOCA secondary to myocardial infarction with posterior spontaneous thrombolysis, in which the clinical presentation was typical, however the coronary angiography showed non obstructive lesions. Therefore, another complementary imaging methods were needed such as the cardiac magnetic resonance.

Neuroendocrine System Regulatory Mechanisms: Acute Coronary Syndrome and Stress Hyperglycaemia.

Neurohormonal systems are activated in the early phase of acute coronary syndromes to preserve circulatory homeostasis, but prolonged action of these stress hormones might be deleterious. Cortisol reaches its peak at 8 hours after the onset of symptoms, and individuals who have continued elevated levels present a worse prognosis. Catecholamines reach 100-1,000-fold their normal plasma concentration within 30 minutes of ischaemia, therefore inducing the propagation of myocardial damage. Stress hyperglycaemia induces inflammation and endothelial dysfunction, and also has procoagulant and prothrombotic effects. Patients with hyperglycaemia and no diabetes elevated in-hospital and 12-month mortality rates. Hyperglycaemia in patients without diabetes has been shown to be an appropriate independent mortality prognostic factor in this type of patient.