- Primary Angioplasty: A Practical Guide: Physiological Lesion Assessment in STEMI and Other Acute Coronary Syndromes [BOOK]
- BOOKSpringer: Singapore
- Invasive coronary physiology is a key instrument in decision-making for the interventional cardiologist. Fractional flow reserve has been well validated in chronic stable coronary artery disease. Its…
Invasive coronary physiology is a key instrument in decision-making for the interventional cardiologist. Fractional flow reserve has been well validated in chronic stable coronary artery disease. Its practical applications have expanded into other clinical situations such as acute coronary syndrome (ACS) including ST-elevation myocardial infarction (STEMI). Recently, other invasive indices of coronary physiology including instantaneous wave-free ratio (iFR), index of microvascular resistance (IMR), hyperemic stenosis resistance (HSR), and coronary flow reserve (CFR) have been explored in the context of ACS. This review will focus on the fundamentals and role of physiologic lesion assessment in the ACS patient.
- Biomarkers of Inflammation in Left Ventricular Diastolic Dysfunction. [Review]
- DMDis Markers 2019; 2019:7583690
- Left ventricular diastolic dysfunction (LVDD) is an important precursor to many different cardiovascular diseases. Diastolic abnormalities have been studied extensively in the past decade, and it has…
Left ventricular diastolic dysfunction (LVDD) is an important precursor to many different cardiovascular diseases. Diastolic abnormalities have been studied extensively in the past decade, and it has been confirmed that one of the mechanisms leading to heart failure is a chronic, low-grade inflammatory reaction. The triggers are classical cardiovascular risk factors, grouped under the name of metabolic syndrome (MetS), or other systemic diseases that have an inflammatory substrate such as chronic obstructive pulmonary disease. The triggers could induce myocardial apoptosis and reduce ventricular wall compliance through the release of cytokines by multiple pathways such as (1) immune reaction, (2) prolonged cell hypoxemia, or (3) excessive activation of neuroendocrine and autonomic nerve function disorder. The systemic proinflammatory state causes coronary microvascular endothelial inflammation which reduces nitric oxide bioavailability, cyclic guanosine monophosphate content, and protein kinase G (PKG) activity in adjacent cardiomyocytes favoring hypertrophy development and increases resting tension. So far, it has been found that inflammatory cytokines associated with the heart failure mechanism include TNF-α, IL-6, IL-8, IL-10, IL-1α, IL-1β, IL-2, TGF-β, and IFN-γ. Some of them could be used as diagnosis biomarkers. The present review aims at discussing the inflammatory mechanisms behind diastolic dysfunction and their triggering conditions, cytokines, and possible future inflammatory biomarkers useful for diagnosis.
- Coronary microvascular dysfunction: a key step in the development of uraemic cardiomyopathy? [Review]
- HHeart 2019 Jun 25
- The syndrome of uraemic cardiomyopathy, characterised by left ventricular hypertrophy, diffuse fibrosis and systolic and diastolic dysfunction, is common in chronic kidney disease and is associated w…
The syndrome of uraemic cardiomyopathy, characterised by left ventricular hypertrophy, diffuse fibrosis and systolic and diastolic dysfunction, is common in chronic kidney disease and is associated with an increased risk of cardiovascular morbidity and mortality. The pathophysiological mechanisms leading to uraemic cardiomyopathy are not fully understood. We suggest that coronary microvascular dysfunction may be a key mediator in the development of uraemic cardiomyopathy, a phenomenon that is prevalent in other myocardial diseases that share phenotypical similarities with uraemic cardiomyopathy such as hypertrophic cardiomyopathy and heart failure with preserved ejection fraction. Here, we review the current understanding of uraemic cardiomyopathy, highlight different methods of assessing coronary microvascular function and evaluate the current evidence for coronary microvascular dysfunction in chronic kidney disease.
- Microvascular spasm in non-ST-segment elevation myocardial infarction without culprit lesion (MINOCA). [Journal Article]
- CRClin Res Cardiol 2019 Jun 24
- CONCLUSIONS: Coronary microvascular spasm is frequently found in patients with NSTEMI without culprit lesion and represents a likely cause of myocardial injury. ACH-testing is useful for detection of vasomotor disorders allowing tailored treatment with calcium antagonists and/or nitrates in addition to secondary prevention to improve symptoms and prognosis. Microvascular spasm in non-ST-segment elevation myocardial infarction without culprit lesion (MINOCA) .
- Non-ST-Elevation Myocardial Infarction-Like Syndrome in Scombroid Tuna Fish Poisoning. [Journal Article]
- AJAm J Cardiol 2019 May 28
- Mistreated fish products ingestion can lead to a histaminergic illness known as Scombroid Syndrome (SS). The disease usually causes cutaneous rash, stomach cramps, nausea, vomiting, breathing disorde…
Mistreated fish products ingestion can lead to a histaminergic illness known as Scombroid Syndrome (SS). The disease usually causes cutaneous rash, stomach cramps, nausea, vomiting, breathing disorder and further histamine-related symptoms. To date, however, SS has been disregarded among the potential triggers of acute coronary syndrome (ACS), in spite of prior published occasional case reports. In the present study we describe 3 consecutive patients presenting with signs and symptoms of ACS associated to SS. Two men and a woman with no history of coronary artery disease and food allergy were studied. Clinical characteristics, electrocardiographic presentation and outcomes are described. Non-ST-elevation myocardial infarction-like pattern was observed in all patients. The 2 men underwent unremarkable coronary angiography, whereas the woman was just monitored at emergency department. All individuals had uneventful follow-up. The present study confirms non-ST-elevation myocardial infarction-like ACS as a possible histaminergic toxic, not allergic, epiphenomenon of mistreated raw tuna fish ingestion, likely due to transient epicardial and/or microvascular coronary vasospasm.
- Retinal Vascular Density as A Novel Biomarker of Acute Renal Injury after Acute Coronary Syndrome. [Journal Article]
- SRSci Rep 2019 May 30; 9(1):8060
- Iodinated contrast agent (ICA)-induced acute kidney injury (AKI) following acute coronary syndrome (ACS) is a frequent complication, which may lead to chronic kidney disease and increased mortality. …
Iodinated contrast agent (ICA)-induced acute kidney injury (AKI) following acute coronary syndrome (ACS) is a frequent complication, which may lead to chronic kidney disease and increased mortality. Optical coherence tomography angiography (OCT-A) of the retina is new tool delivering a rapid and noninvasive assessment of systemic microvascularization, which is potentially involved in the occurrence of ICA-induced AKI. Between October 2016 and March 2017, 452 ACS patients were admitted to our cardiac intensive care unit. OCT-A was performed within 48 h after the ICA injection. Patients with a history of retinal disease were excluded. The patients included were divided into two groups depending on whether or not AKI occurred after injection of ICA, according to KDIGO criteria. Of the 216 patients included, 21 (10%) presented AKI. AKI was significantly associated with age, Mehran score, GRACE score, and NT-proBNP. AKI patients had significantly lower retinal vascular density (RVD)) and had more frequent low RVD (81% vs 45%, P = 0.002). Adding low RVD to the Mehran score and the NT-proBNP, or to the GRACE score and the NT-proBNP, significantly improved their predictive values, suggesting that systemic microvascular involvement remains incompletely addressed by either standard risk scores or factors known to be associated with ICA-induced AKI.
- Arterial Stiffness in the Heart Disease of CKD. [Journal Article]
- JAJ Am Soc Nephrol 2019; 30(6):918-928
- CKD frequently leads to chronic cardiac dysfunction. This complex relationship has been termed as cardiorenal syndrome type 4 or cardio-renal link. Despite numerous studies and reviews focused on the…
CKD frequently leads to chronic cardiac dysfunction. This complex relationship has been termed as cardiorenal syndrome type 4 or cardio-renal link. Despite numerous studies and reviews focused on the pathophysiology and therapy of this syndrome, the role of arterial stiffness has been frequently overlooked. In this regard, several pathogenic factors, including uremic toxins (i.e., uric acid, phosphates, endothelin-1, advanced glycation end-products, and asymmetric dimethylarginine), can be involved. Their effect on the arterial wall, direct or mediated by chronic inflammation and oxidative stress, results in arterial stiffening and decreased vascular compliance. The increase in aortic stiffness results in increased cardiac workload and reduced coronary artery perfusion pressure that, in turn, may lead to microvascular cardiac ischemia. Conversely, reduced arterial stiffness has been associated with increased survival. Several approaches can be considered to reduce vascular stiffness and improve vascular function in patients with CKD. This review primarily discusses current understanding of the mechanisms concerning uremic toxins, arterial stiffening, and impaired cardiac function, and the therapeutic options to reduce arterial stiffness in patients with CKD.
- The role of androgens in microvascular endothelial dysfunction in polycystic ovary syndrome: does size matter? [Journal Article]
- JPJ Physiol 2019; 597(11):2829-2830
- Coronary microvascular dysfunction in patients with acute coronary syndrome and no obstructive coronary artery disease. [Journal Article]
- CRClin Res Cardiol 2019 Mar 29
- CONCLUSIONS: Patients with NSTE-ACS and NO-CAD exhibit a significant coronary dysfunction, which seems to involve both an increased constrictor reactivity, likely mainly involving coronary microcirculation, and a reduced microvascular dilator function, both persisting at 12-month follow-up.
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- HbA1c: High in acute cerebral infarction and low in brain trauma. [Journal Article]
- PMProg Mol Biol Transl Sci 2019; 162:293-306
- HbA1c is a glycated hemoglobin. The ≥6.5% HbA1c in total hemoglobins has been used in diagnosing and guiding therapy for patients with diabetes since 1970s. Increased HbA1c levels are observed in oth…
HbA1c is a glycated hemoglobin. The ≥6.5% HbA1c in total hemoglobins has been used in diagnosing and guiding therapy for patients with diabetes since 1970s. Increased HbA1c levels are observed in other nondiabetic conditions, such as cancers, uremia, macro- and microvascular diseases. However, a systematic comparison of the HbA1c levels in different types of human diseases has not been reported. In current study, 48,183 clinical lab test results of HbA1c levels from healthy individuals and patients with 36 different types of diseases during the past 5 years in our hospital were retrieved and analyzed. Based on the mean (SD), median, and p (-Log10p) values, we found that patients suffering type 2 diabetes, acute cerebral infarction, nephrotic syndrome, endometrial cancer, cerebral ischemia, leukemia, bladder cancer, chronic obstructive pulmonary disease plus other 27 diseases had significantly (p<0.05, -Log10p>1.30) increased HbA1c levels, whereas patients suffering brain trauma had significantly decreased HbA1c levels compared to that of healthy controls. Moreover, the highest -Log10p values were observed in type 2 diabetes, acute cerebral infarction, coronary heart disease, cerebrovascular disease, healthy controls >65 years old, and diabetic nephropathy, indicating the increased HbA1c levels were associated with aging and aging-related diseases. Unexpectedly, 29/36 diseases had both mean and median HbA1c levels ≥6.5%. These data suggested that the increased HbA1c levels were a common feature of nondiabetic diseases. Revealing the molecular mechanisms underlying the data presented in current study might help better understand the meaning of glycemic control.