Worldwide, cardiovascular diseases (CVDs) represent one of the main causes of morbidity and mortality, and acute coronary syndromes are responsible for a large number of sudden cardiac deaths. One of the main challenges that still exist in this area is represented by the early detection and targeted monitoring of the pathophysiology involved in CVDs. During the last couple of years, researchers have highlighted the importance of molecular and epigenetic mechanisms involved in the initiation and augmentation of CVDs, culminating in their most severe form represented by acute myocardial infarction. One of the most studied molecular factors involved in this type of pathology is represented by nuclear transcription factor kappa B (NF-κB), as well as the involvement of microRNAs (miRNAs). It has been suggested that miRNAs can also be involved in the complex process of atheromatous plaque vulnerabilization that leads to an acute cardiac event. In this review paper, we describe the most important molecular mechanisms involved in the pathogenesis of CVDs and atheromatous plaque progression and vulnerabilization, which include molecular mechanisms dependent on NF-κB. For this paper, we used international databases (PubMed and Scopus). The keywords used for the search were “miRNAs biomarkers”, “miRNAs in cardiovascular disease”, “NF-κB in cardiovascular disease”, “molecular mechanism in cardiovascular disease”, and “myocardial NF-κB mechanisms”. Numerous molecular reactions that have NF-κB as a trigger are involved in the pathogenesis of CVDs. Moreover, miRNAs play an important role in initiating and aggravating certain segments of CVDs. Therefore, miRNAs can be used as biomarkers for early evaluation of CVDs. Furthermore, in the future, miRNAs could be used as a targeted molecular therapy in order to block certain mechanisms responsible for inducing CVDs and leading to acute cardiovascular events.

A hypertensive crisis is an abrupt and severe rise in the arterial blood pressure (BP) occurring either in patients with known essential or secondary hypertension, or it may develop spontaneously. The most frequent cause for the severe and sudden increase in BP is inadequate dosing or stopping antihypertensive treatment in hypertensive patients. Severe hypertension can be defined as either a hypertensive emergency or an urgency, depending on the existence of organ damage. In hypertensive urgencies, there are no signs of acute end-organ damage, and orally administered drugs might be sufficient. In hypertensive emergencies, signs of acute end-organ damage are present, and in these cases, quickly-acting parenteral drugs must be used. The prompt recognition, assessment, and treatment of hypertensive urgencies and emergencies can decrease target organ damage and mortality. In this review, the definitions and therapeutic recommendations in a hypertensive crisis are presented in the light of the 2017 ACC/AHA Hypertension Guidelines.

Background: The independent role of each plaque feature in relation to plaque vulnerability is still the subject of ongoing research. This study aimed to compare the morphologic characteristics of vulnerable atheromatous coronary plaques with the ones of stable, non-vulnerable plaques, and in plaques with different locations in the coronary tree, in order to identify the most relevant imaging-based biomarkers associated with coronary plaque vulnerability. Material and methods: This was a prospective observational, non-randomized study that included 50 patients with unstable angina who underwent computed tomography angiography for assessment of the entire coronary artery tree followed by complex morphologic analysis of all lesions, divided into two groups: group 1 – 25 patients with vulnerable plaque (VP) and group 2 – 25 age- and gender-matched patients with non-vulnerable plaque (NVP). Results: Lesions with a stenosis degree >70% were significantly longer than those with a stenosis degree <70% (8.27 ± 2.74 mm vs. 5.56 ± 4.11 mm, p = 0.04). VP presented significantly higher values of plaque thickness (p = 0.0005), plaque burden (p = 0.0004), and higher total plaque volume (p = 0.0005) than NVP. The remodeling index was not significantly different between the groups (p = 0.6), but the eccentricity index was (0.24 ± 0.14 compared to 0.14 ± 0.17, p = 0.023). Linear regression analysis revealed a significant correlation between plaque burden and plaque components in VP (r = 0.76, p <0.0001 for necrotic core; r = 0.62, p = 0.0008 for fibro-fatty tissue; and r = 0.5, p = 0.01 for fibrotic tissue volume). Culprit plaques located in the right coronary artery presented significantly larger plaque burden volumes (91.17 ± 4.88 mm3 vs. 83.35 ± 8.47 mm3, p = 0.04), larger volumes of necrotic core (82.03 ± 47.85 mm3 vs. 45.84 ± 43.72 mm3, p = 0.02) and fibrofatty tissue (53.23 ± 31.92 mm3 vs. 23.76 ± 20.90 mm3, p = 0.02) than the ones situated in the left coronary artery. Conclusions: VPs from the culprit lesions exhibit a different phenotype than non-vulnerable ones, and vulnerability features are present in a significantly larger extent in VPs from the right coronary artery as compared to those from the left coronary artery.

Introduction: Cardiovascular disease is the leading cause of death among women irrespective of race or ethnicity, and about half of these deaths are caused by coronary artery disease. Several studies have reported that cardiovascular diseases manifest themself with a delay of about 7–10 years in women and that they have higher in-hospital mortality. It has not yet been established whether female gender itself, through biological and sociocultural differences, represents a risk factor for early in-hospital mortality in ST-segment elevation acute myocardial infarction (STEMI). The aim of our study was to identify the angiographic particularities in women with STEMI from North East Romania. Material and Methods: For one year, 207 (31.7%) women and 445 (68.3%) men diagnosed with acute myocardial infarction were hospitalized in the Cardiology Clinic of the “Prof. Dr. George I. M. Georgescu” Institute of Cardiovascular Diseases in Iași, Romania. Results: The highest incidence of symptom onset was between 6:00 a.m. and 12:00 a.m., this morning polarization being more obvious in women. Within the first two hours of admission to the hospital, coronary angiography was performed in 78.1% of men and only 67.3% of women, the difference being statistically significant (p <0.05). We found that a large number of women had multivascular coronary disease (47.9% vs. 42.3%). At the same time, we found that left main disease and multivascular disease were more frequent in women than in men (3.8% vs. 0.7%, p = 0.001 for left main plus two-vessel disease, and 19.4% vs. 14.8%, p = 0.0005 for three-vessel disease). Conclusions: In women, coronary events began more frequently in the morning, with atypical symptoms; also, fewer women presented to the hospital within the first 12 hours after the onset of the acute event. Compared to men, women from North East Romania present a higher incidence of multivascular atherosclerotic coronary lessions, indicating a higher severity of STEMI in the female population from this geographical area.

A 56-year-old man presented to the emergency department with pain, swelling, and restricted mobility of the left lower limb and shortness of breath on exertion in the previous 3 days. Seven months prior to this presentation, he had been diagnosed with adult-onset Still’s disease based on the Yamuguchi criteria, after excluding the presence of any other disease. The patient had been treated with prednisolone and methotrexate. Subsequent investigations revealed that he developed bilateral deep venous thrombosis and bilateral pulmonary emboli. This case emphasizes that adult-onset Still’s disease can be a rare but life-threatening cause of venous thromboembolism.

Introduction: We present the case of a young man with multiple atherosclerotic risk factors and a rare cause of angina and supraventricular ectopic beats. Case presentation: A 35-year-old man with one-year history of stable angina pectoris and supraventricular ectopic beats, without any medication, presented to the emergency room complaining of anterior chest pain that occurs at moderate physical exertion. The rest electrocardiogram, transthoracic echocardiography, and chest X-ray were normal; the exertion stress test was also normal, except for supraventricular ectopic beats (trigeminal rhythm). Due to the intermediate pre-test probability of coronary artery disease, he was evaluated using coronary computed tomography angiography. An anomalous origin of the right coronary artery from the left coronary sinus, with an inter-arterial course and without any atheroma plaques, was observed. During hospitalization the evolution was stable, without complications. The patient was further referred to a cardiac surgery clinic to evaluate the possibility of surgical treatment of this anomaly. Conclusions: Coronary artery anomalies are very rare; however, they present multiple implications in current practice. The most severe complication of this condition is represented by sudden death in young patients due to malignant ventricular arrhythmias. Imaging diagnostic techniques allow for a rapid, noninvasive diagnosis of this rare cause of angina.