Many lesions in patients undergoing percutaneous coronary intervention (PCI) exhibit significant calcification. Several techniques have been developed to improve outcomes in this setting. However, their impact on coronary microcirculation remains unknown. The aim of this study is to evaluate the influence of plaque modification techniques on coronary microcirculation across patients with severely calcified coronary artery disease. In this multicenter retrospective study, consecutive patients undergoing PCI with either Rotablation (RA) or Shockwave-intravascular-lithotripsy (IVL) were included. Primary endpoint was the impairment of coronary microvascular resistances assessed by Δ angiography-derived index of microvascular resistance (ΔIMRangio) which was defined as the difference in IMRangio value post- and pre-PCI. Secondary endpoints included the development of peri procedural PCI complications (flow-limiting coronary dissection, slow-flow/no reflow during PCI, coronary perforation, branch occlusion, failed PCI, stroke and shock developed during PCI) and 12-month follow-up adverse events. 162 patients were included in the analysis. Almost 80% of patients were male and the left descending anterior artery was the most common treated vessel. Both RA and IVL led to an increase in ΔIMRangio (22.3 and 10.3; p = 0.038, respectively). A significantly higher rate of PCI complications was observed in patients with ΔIMRangio above the median of the cohort (21.0% vs. 6.2%; p = 0.006). PCI with RA was independently associated with higher ΔIMRangio values (OR 2.01, 95% CI: 1.01-4.03; p = 0.048). Plaque modification with IVL and RA during PCI increases microvascular resistance. Evaluating the microcirculatory status in this setting might help to predict clinical and procedural outcomes and to optimize clinical results.

BACKGROUND: Preservation of organ function and viability is a crucial factor for survival in cardiogenic shock (CS) patients. There is not information enough on cytoprotective substances that may delay organs damage in CS. We hypothesize that cytidine-5-diphosphocholine (CDP-choline) can act as a cytoprotective pharmacological measure that diminishes the target organ damage. So, we aimed to perform a review of works carried out in our institution to evaluate the effect of therapeutic cytoprotection of the CDP-choline.
CONCLUSIONS: CDP-choline is an intermediate metabolite in the synthesis of phosphatidylcholine. It is also a useful drug for the treatment of acute ischaemic stroke, traumatic brain injury, and neurodegenerative diseases and has shown an excellent pharmacological safety profile as well. We review our institution\'s work and described the cytoprotective effects of CDP-choline in experimental models of heart, liver, and kidney acute damage, where this compound was shown to diminish reperfusion-induced ventricular arrhythmias, oxidative stress, apoptotic cell death, inflammation, lactic acid levels and to preserve mitochondrial function.
CONCLUSIONS: We propose that additional research is needed to evaluate the impact of cytoprotective therapy adjuvant to mitigate target organ damage in patients with CS.

UNASSIGNED: ST-segment elevation myocardial infarction (STEMI) has traditionally been managed with immediate reperfusion of the culprit artery, primarily through percutaneous coronary intervention and stent placement. Emerging data are highlighting the crucial importance of post-infarct microcirculatory function assessment.
UNASSIGNED: This report presents a patient with an inferior STEMI who was successfully reperfused without stent implantation. Tools such as optical coherence tomography, fractional flow reserve, and positron emission tomography computed tomography N-13 ammonia were utilized, offering comprehensive insights into the anatomical and functional characteristics of both the epicardial vessel and microcirculation.
UNASSIGNED: The recovery of the reversible component of microcirculatory dysfunction, observable as early as 5 days post-infarction, might carry significant implications for clinical decision-making. Such insights can potentially influence contemporary treatment strategies, including the consideration of deferred stenting. This case underscores the significance of post-infarct microcirculatory function and its potential impact on therapeutic approaches.

Background: Ischemic stroke is a leading cause of mortality and disability worldwide. Microcirculatory dysfunction is the foremost hindrance for a good clinical prognosis in ischemic stroke patients. Clinical researches show that Chuanzhitongluo capsule (CZTL) has a curative effect during the recovery period of ischemic stroke, which contributes to a good prognosis. However, it is not known whether CZTL treats ischemic stroke by ameliorating microcirculation dysfunction. Objective: In this study, we investigated the influence of CZTL on microcirculation and its underlying mechanism. Methods: A rat model of acute microcirculatory dysfunction was established by stimuli of adrenaline and ice water. The microcirculatory damage in model rats and the efficacy of CZTL were assessed by detecting laser speckle contrast imaging, coagulation function, hemorheology, vasomotor factor and microcirculation function. The potential mechanism of CZTL action was explored by the untargeted metabolomic analysis based on ultra-performance liquid chromatography-quadrupole-time of flight-mass spectrometry. Results: Laser speckle contrast imaging showed that model rats suffered low perfusion in ears, feet and tails, and CZTL treatment increased microcirculatory blood flow. Coagulation function detection results showed that CZTL diminished the reduction of thrombin time, prothrombin time, activated partial thromboplastin time and the elevated fibrinogen level caused by acute microcirculatory dysfunction. Furthermore, CZTL could recover the increased blood viscosity as well as the abnormal vasomotor and microcirculation function in rats with acute microcirculatory dysfunction. Metabolomics analysis indicated that CZTL might regulate sphingolipid metabolism and arachidonic acid metabolism to exert protective effects on microcirculation. Conclusion: These results elucidated that CZTL was highly effective against microcirculatory dysfunction and its potential mechanisms related with the modulation of sphingolipid and arachidonic acid metabolic pathways. The present study provided a new perspective on the clinical application of CZTL, and it contribute to explore novel therapeutic drug against microcirculatory dysfunction.

Sepsis-associated AKI is a life-threatening complication that is associated with high morbidity and mortality in patients who are critically ill. Although it is clear early supportive interventions in sepsis reduce mortality, it is less clear that they prevent or ameliorate sepsis-associated AKI. This is likely because specific mechanisms underlying AKI attributable to sepsis are not fully understood. Understanding these mechanisms will form the foundation for the development of strategies for early diagnosis and treatment of sepsis-associated AKI. Here, we summarize recent laboratory and clinical studies, focusing on critical factors in the pathophysiology of sepsis-associated AKI: microcirculatory dysfunction, inflammation, NOD-like receptor protein 3 inflammasome, microRNAs, extracellular vesicles, autophagy and efferocytosis, inflammatory reflex pathway, vitamin D, and metabolic reprogramming. Lastly, identifying these molecular targets and defining clinical subphenotypes will permit precision approaches in the prevention and treatment of sepsis-associated AKI.

Early brain injury (EBI) is considered an important cause of morbidity and mortality after aneurysmal subarachnoid hemorrhage (aSAH). As a factor in EBI, microcirculatory dysfunction has become a focus of interest, but whether microcirculatory dysfunction is more important than angiographic vasospasm (aVS) remains unclear. Using data from 128 cases, we measured the time to peak (TTP) in several regions of interest on digital subtraction angiography. The intracerebral circulation time (iCCT) was obtained between the TTP in the ultra-early phase (the baseline iCCT) and in the subacute phase and/or at delayed cerebral ischemia (DCI) onset (the follow-up iCCT). In addition, the difference in the iCCT was calculated by subtracting the baseline iCCT from the follow-up iCCT. Univariate analysis showed that DCI was significantly increased in those patients with a prolonged baseline iCCT, prolonged follow-up iCCT, increased differences in the iCCT, and with severe aVS. Poor outcome was significantly increased in patients with prolonged follow-up iCCT and increased differences in the iCCT. Multivariate analysis revealed that increased differences in the iCCT were a significant risk factor that increased DCI and poor outcome. The results suggest that the increasing microcirculatory dysfunction over time, not aVS, causes DCI and poor outcome after aneurysmal aSAH.

OBJECTIVE: This article reviews the pathological mechanisms and progress of imaging of severe frostbite to assist in the search for targets for clinical diagnosis and treatment of severe frostbite. This review also aims to provide strong evidence for clinical diagnosis and treatment of deep frostbite.
METHODS: The review was based on the summary and analysis of the existing literature, and explored the pathological mechanism of deep frostbite and the advantages and disadvantages of imaging diagnostic methods.
RESULTS: According to the depth of tissue involvement, frostbite is divided into 4 levels. Severe frostbite includes Grade 3 and Grade 4 frostbite. Clinical performance evaluation and imaging diagnostic research have always been the mainstream of severe frostbite diagnosis. Imaging methods focus on vascular patency and tissue vitality. This article introduces angiography, SETCT/CT and MRA, and we summarize the advantages and disadvantages of these imaging methods. We recommend corresponding imaging modalities according to the state of frostbite patients.
CONCLUSIONS: Imaging examination, especially angiography and bone scans, provide useful information for determining the diagnosis and prognosis of severe frostbite. In order to obtain a good clinical prognosis, clinicians should first perform SPECT/CT. MRA does not burden the patient\'s body, but the balance between cost and benefit must be considered. Angiography provides a good feedback on the changes in blood vessel status before and after treatment, which is helpful for discovering the response of limbs to treatment.

Myocardial ischemia constitutes one of the most important pathophysiological features in hypertrophic cardiomyopathy. Chronic and recurrent myocardial ischemia leads to fibrosis, which may culminate in myocardial dysfunction. Since the direct visualization of coronary microcirculation in vivo is not possible, its function must be studied indirectly. Invasive and noninvasive techniques allow microcirculatory dysfunction to be evaluated, including echocardiography, magnetic resonance, positron emission tomography, and cardiac catheterization. Blunted myocardial blood flow and coronary flow reserve have been suggested to associate with unfavorable prognosis. Microcirculatory dysfunction may be one additional important parameter to take into account for risk stratification beyond the conventional risk factors.

In spite of a remarkable decline in death rates from cardiovascular disease (CVD) observed over the last decades, CVD still remains the leading cause of mortality in both men and women worldwide. Overall the age-adjusted CVD mortality and morbidity rates are highest in men than in women. However, the risk of CVD in women should not be underestimated given that approximately one of two women in developed countries will die of mostly preventable heart diseases or stroke. Although men and women share the same cardiovascular risk factors, there are substantial sex differences in the first manifestation and clinical presentation of CVD. In this part of the chapter, we will discuss the recent epidemiological data on sex discrepancies in the prevalence and burden of different CVDs.

Venous ulcers are a common chronic problem in many countries especially in Northern Europe and USA. The overall prevalence of this condition is 1% rising to 3% in the over 65 years of age. Over the last 25 years, there have been many developments applicable to its diagnosis and treatment. These advances, notwithstanding healing response and recurrence, are variable, and the venous ulcer continues to be a clinical challenge. The pathogenesis of venous ulcers is unrelieved or ambulatory venous hypertension resulting mostly from deep venous thrombosis leading to venous incompetence, lipodermatosclerosis, leucocyte plugging of the capillaries, tissue hypoxia and microvascular dysfunction. It is not known what initiates venous ulcers. Triggers vary from trauma of the lower extremity to scratching to relieve itchy skin over the ankle region. Venous ulcers can be painful, and this condition presents an increasing burden of care. A systematic analysis of the role of technology used for diagnosis and management strongly supports the use of compression as a mainstay of standardised care. It further shows good evidence for the potential of some treatment procedures to accelerate healing. This article reviews the pathogenetic mechanisms, current diagnostic methods and standard care and its limitations.