Migrating Localized ST-Segment Elevation With Ongoing Chest Pain.

A patient in their 60s presented with a 6-hour history of sudden-onset worsening chest pain associated with shortness of breath and diaphoresis. What is your diagnosis?

Intravascular Sono-Ablation for In-Stent Restenosis Relief: Transducer Development and the In-Vitro Demonstration.

OBJECTIVE: This study aimed to propose a new clinical modality for the relief of in-stent restenosis (ISR) using focused ultrasound (FUS) ablation. In the first research stage, a miniaturized FUS device was developed for the sonification of the remaining plaque after stenting, known as one of the causes of ISR. METHODS: This study presents a miniaturized (<2.8 mm) intravascular FUS transducer for ISR treatment. The performance of the transducer was predicted through a structural-acoustic simulation, followed by fabrication of the prototype device. Using the prototype FUS transducer, we demonstrated tissue ablation with bio-tissues over metallic stents, mimicking in-stent tissue ablation. Next, we conducted a safety test by detecting the existence of thermal damage to the arterial tissue upon sonication with a controlled dose. RESULTS: The prototype device successfully delivered sufficient acoustic intensity (>30 W/cm2) to a bio tissue (chicken breast) through a metallic stent. The ablation volume was approximately 3.9 × 7.8 × 2.6 mm3. Furthermore, 1.5 min sonication was sufficient to obtain an ablating depth of approximately 1.0 mm, not thermally damaging the underlying artery vessel. CONCLUSION: We demonstrated in-stent tissue sonoablation, suggesting it could be as a future ISR treatment modality. SIGNIFICANCE: Comprehensive test results provide a key understanding of FUS applications using metallic stents. Furthermore, the developed device can be used for sonoablation of the remaining plaque, providing a novel approach to the treatment of ISR.

A Paradoxical ST-Segment Elevation Distribution Rendering a Challenging Prediction of the Culprit Vessel in Acute Myocardial Infarction.

This case report describes a patient in their 50s with sudden-onset chest pain.

Photoplethysmographic imaging and analysis of pulsatile pressure wave in palmar artery at 10 wavelengths.

Significance: As a noncontact method, imaging photoplethysmography (iPPG) may provide a powerful tool to measure pulsatile pressure wave (PPW) in superficial arteries and extract biomarkers for monitoring of artery wall stiffness. Aim: We intend to develop a approach for extraction of the very weak cardiac component from iPPG data by identifying locations of strong PPW signals with optimized illumination wavelength and determining pulse wave velocity (PWV). Approach: Monochromatic in vivo iPPG datasets have been acquired from left hands to investigate various algorithms for retrieval of PPW signals, distribution maps and waveforms, and their dependence on arterial location and wavelength. Results: A robust algorithm of pixelated independent component analysis (pICA) has been developed and combined with spatiotemporal filtering to retrieve PPW signals. Spatial distributions of PPW signals have been mapped in 10 wavelength bands from 445 to 940 nm and waveforms were analyzed at multiple locations near the palmar artery tree. At the wavelength of 850 nm selected for timing analysis, we determined PWV values from 12 healthy volunteers in a range of 0.5 to 5.8 m/s across the hand region from wrist to midpalm and fingertip. Conclusions: These results demonstrate the potentials of the iPPG method based on pICA algorithm for translation into a monitoring tool to characterize wall stiffness of superficial artery by rapid and noncontact measurement of PWV and other biomarkers within 10 s.

Multimodality delineation of a fistulous ruptured sinus of Valsalva aneurysm: a teaching case report.

Background: Ruptured sinus of Valsalva (SOV) is a rare cardiac anomaly with poor prognosis if untreated. Early diagnosis with accurate delineation of its anatomy is critical for timely treatment and choice of surgical vs. percutaneous intervention. Here we report a case of fistulous rupture of SOV; the preoperative multimodality studies including echocardiography, cardiac magnetic resonance and cardiac catheterization provided teaching and learning points. Case summary: A 48-year-old man with history of heart murmur and hypertension presented with a 5-day history of shortness of breath and peripheral oedema. He was diagnosed with rapid atrial flutter. The transthoracic and transesophageal echocardiography showed severe biventricular systolic dysfunction with a left-to-right shunt from ruptured SOV. The colour Doppler by transthoracic and transesophageal echocardiography and cardiac magnetic resonance revealed a swaying shunt flow exiting in direction to the right atrium (RA) and basal right ventricle (RV) during systole and diastole with no myocardial scaring. The left and right heart catheterization showed elevated right-sided pressures, pulmonary capillary wedge pressure, and left ventricular end-diastolic pressure. There was no difference in O2 saturation between venae cavae and RA but a misleading step-up in O2 saturation between RA and RV. Owing to rupture anatomy with uncertainty, the patient underwent surgical intervention. The ruptured SOV tunnelled through the base of tricuspid annulus to the RA very close to the basal RV. Discussion: Even with multimodality studies it can still be challenging to delineate the anatomy of a ruptured SOV without uncertainty preoperatively.

Cholesterol Paradigm and Beyond in Atherosclerotic Cardiovascular Disease: Cholesterol, Sterol Regulatory Element-Binding Protein, Inflammation, and Vascular Cell Mobilization in Vasculopathy.

Hypercholesterolemia is a well-established risk factor for atherosclerotic cardiovascular disease (ASCVD). How cholesterol and its carrier lipoproteins are involved in ASCVD is still under extensive investigation. Satins are thus far the best-proven class of cholesterol-lowering medications to improve the clinical outcomes of ASCVD. Statins specifically inhibit the rate-limiting enzyme 3-hydroxy-3-methylglutaryl-CoA reductase of the mevalonate pathway for cholesterol biosynthesis. The widely accepted theory is that statins inhibit the hepatic cholesterol synthesis causing upregulation of hepatocyte low-density lipoprotein (LDL) receptor; receptor-mediated LDL uptake and metabolism in the liver results in reduction of circulating LDL cholesterol, which subsequently reduces vascular deposition and retention of cholesterol or LDL in atherogenesis. Nevertheless, cholesterol biosynthesis is ubiquitous, also in extrahepatic cells including those in vascular wall, under tight regulation by sterol regulatory element-binding protein (SREBP), the master gene transcription factor governing cholesterol biosynthesis. Studies have shown that SREBP can be upregulated in vascular wall subject to injury or stent implantation. SREBP can be activated by proinflammatory and mitogenic factors in vascular cells, leading to hyperactive mevalonate pathway, which promotes vascular cell mobilization, further proinflammatory and mitogenic factor release from vascular cells, and vascular inflammation. In this article, we review the cellular cholesterol homeostasis regulation by SREBP and SREBP-mediated vascular hyperactive cholesterol biosynthesis, we term vascular hypercholesterolism, in the pathogenesis of ASCVD and vasculopathy. SREBP functions as a platform bridging cholesterol, inflammation, and vascular cell mobilization in ASCVD pathogenesis. Targeting vascular hypercholesterolism could open a new avenue in fighting against ASCVD.