A fractal physics explanation for acute thrombotic occlusion in an apparently healthy coronary arteryThe acute arterial occlusion of an artery that has no significant preexistent lesions leads to dramatic consequences due to the lack of collateral substitutive circulation, as this kind of circulation usually develops within years in the presence of hemodynamic significant stenosis (1).Classical models which explain this phenomenon take into account the cracking of an intimal atheroma plaque, the activation of the prothrombogenic cascade through the denudation of the endothelium, and the formation of a completely occlusive thrombus in certain circumstances (2, 3). At least one counterargument should be considered: Why does an occlusive thrombus form so quickly in the absence of a stenosis when the sanguine flux is unaltered? Why the "wash-out'' phenomenon does not appear?Without contradicting these usual models, through a fractal model (4, 5), we will prove that the blocking of the lumen of an absolutely healthy artery can happen as a result of the "stopping effect" (even in the absence of disputable cracked and nonprotrusive atheroma plaque), in the conditions of a normal sanguine circulation.Therefore, if we consider blood a Bingham-type rheological fluid, then (1) where is the viscosity tangential unitary effort, is the deformation tangential unitary effort, is the velocity gradient with respect to the normal on the transversal section, and is the viscosity coefficient.Our fractal model (4, 5) was used for in vivo analyses of 10 clinical cases of patients with acute occlusive thrombus on an absolutely healthy artery. These cases were selected during a 2-year period (2013)(2014)(2015). Patients with atrial fibrillation were excluded for preventing mismatch with thromboembolic acute coronary occlusion. Patients with patent foramen ovale (diagnosed by transesophageal echocardiography) were excluded to avoid a paradoxical coronary embolism. Intravascular ultrasound or coronary CT angiography were not performed in these patients; although some irregularities could be seen on angiography, it is clear that there are no significant ulcerated atheroma plaques or major signs of parietal atherosclerosis. Also, in patients >50 years, an absolutely normal coronary wall is more likely a utopia. We performed EKG Holter monitoring in all patients for exclusion of paroxysmal atrial fibrillation.We present here the two most relevant cases (Fig. 1a-h) with thrombus dimensions of ≥60 mm (for the other eight cases, the thrombus dimensions were between 30 and 60 mm). For all the cases, our theoretical results were verified by coronarography images. 1) Patient 1 was a 52-year-old male patient who was diagnosed with acute inferolateral ischemia. Coronary angiography revealed an acute occlusive thrombus (4-4.5 mm diameter and 60-80 mm length) at the junction between segments I and II of the right coronary artery. After thrombus aspiration, a distal thrombotic embolism appeared with an apparently healthy artery (or possible minimal les...
Background: Prevention of sudden cardiac death (SCD) early after acute myocardial infarction (AMI) is still a challenge, without clear recommendations in spite of the high incidence of life-threatening ventricular arrhythmias, as implantable cardiac defibrillator (ICD) placement is not indicated in the first 40 days after an AMI; this timing is aleatory and it is owed to fact that the two pivotal studies for evaluation of ICDs in primary prevention, MADIT and MADIT II, excluded the patients within three, respectively four weeks after AMI. Methods: We conducted a retrospective, single-center study that included 77 patients with AMI. All patients were monitored by continuous ECG in the first week after the event. Transthoracic echocardiography was performed at discharge and 40 days after the event. Patients with ejection fraction of 35% or less as assessed by 2D echocardiography 40 days after the MI, which received an ICD for the primary prevention of SCD, were included in the study. The subjects were followed for a median of 38 months, by means of device interrogation and echocardiography. Results: We divided our patients into two groups: in the first group, with left ventricular ejection fraction (LVEF) under 30% after MI, all patients remained in the reduced ejection fraction heart failure category, with an increase from an initial mean of 18.93 ± 4.99% to a mean of 22.18 ± 4.53% after a period of 40 days; we obtained a positive and statistically significant correlation (p < 0.001 and r -0.547), and all patients presented indication of ICD implant 40 day after MI. In the second group with LVEF between 30% and 35% after MI, the mean LVEF increased from an initial mean of 31.73 ± 1.33% to a mean of 32.33 ± 1.49% after a period of 40 days. A statistically significant correlation (p -0.02 and r -0.78) was obtained, although 3 patients presented a LVEF over 35% at 40 days post-MI. Most of the ICD therapies (14.54%) appeared in patients with LVEF <30% and these patients also presented a higher percentage of NSVT at initial ECG monitoring (54% vs. 50%) and NSVT at ICD interrogation (80% vs. 66.7%); statistical significance was not reached -p > 0.05. The majority of the ICD therapies (11.9% from 13.4%) appeared in patients with NSVT at initial ECG monitoring; also, these presented an increased number of NSVT at ICD interrogation (77.6% vs. 6%) when compared to patients without VT detection at the initial ECG monitoring. Still, statistical significance was not reached -p > 0.15. Conclusions: The patients could benefit from ICD implant earlier than stated in the actual guidelines, since there are insufficient data in the literature for the waiting time of 40 days. Correlated with the increased risk of SCD in the first months post myocardial infarction, the present study proves the benefit of early ICD implantation considering that all our patients with a low ejection fraction immediately after infarction remained in the same category and the great majority (96.1%) required the implantation of an ICD after 40 days. Thus, w...
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