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Intravascular imaging (IVI), including intravascular ultrasound (IVUS) and optical coherence tomography (OCT), is clinically useful for assessing the luminal size, lesion length, and plaque characteristics, as well as for evaluating stent deployment; however, it is not designed to estimate myocardial ischemia accurately. Thus, several types of IVI-derived fractional flow reserve (FFR) (IVI-derived FFR) have been developed and reported. In general, the algorithms of virtual FFR are based on basic fluid dynamics equations (mainly Poiseuille and Borda–Carnot equations) and original microvascular models (fixed velocity or calculating coronary flow reserve). Although the models and assumptions used in the past reports were mostly based on the standard population (not independent patient data), the developed software calculated FFR with high accuracy (88% to 94%) with strong correlations between IVI-derived FFR and wire-based FFR (0.69 to 0.89). Given several other less invasive virtual FFR methods currently available for clinical use, IVI-derived FFR would be limited for the sole use of pre-percutaneous coronary intervention (PCI) physiological evaluation; however, it may play a unique role at PCI guidance and optimization, potentially allowing comprehensive and time/cost-saving assessment of both anatomical and physiological lesion properties using a single diagnostic device.

The slow flow phenomenon is a critical complication during percutaneous coronary intervention (PCI) that leads to poor outcomes. We aimed to evaluate the mechanisms underlying the slow flow phenomenon using intravascular ultrasound (IVUS). We retrospectively analyzed IVUS data from 62 lesions in 58 consecutive patients who experienced the slow flow phenomenon during PCI. IVUS was performed immediately after the development of the slow flow phenomenon to assess its cause. No IVUS-based evidence of mechanical obstruction was categorized as distal embolization. Distal embolization was observed in 46 lesions (74%). The slow flow phenomenon occurred in all these lesions after stent implantation. In addition to distal embolization, three different mechanisms underlying the induction of the slow flow phenomenon due to mechanical obstructions (16 lesions, 26%) were detected on IVUS, namely, medial dissection/hematoma (6 lesions), intimal flap (6 lesions), and thrombus obstruction (4 lesions). Most mechanical obstructions (13 lesions, 81%) could not be identified by angiography alone. In 15/16 lesions (94%) with mechanical obstruction, deteriorated flow improved immediately after balloon dilatation or bail-out stent implantation, although intracoronary vasodilator administration could not reestablish coronary flow. The frequency of mechanical obstruction as the cause of the slow flow phenomenon was relatively high. Given the difficulty in angiographical differentiation, IVUS-guided management of slow flow may be a useful strategy.

Glagov proposed that remodeling delayed development of significant coronary artery stenoses until plaque occupied, on average, 40 of arterial area (40 plaque burden). The aim of the current study was to confirm the previously proposed concept of coronary remodeling as first described by Glagov who studied postmortem left main coronary arteries (LMCAs).

Aims Several studies have demonstrated that type 2 diabetes mellitus (T2DM) is associated with accelerated atherosclerosis, which results in an increased risk of coronary vascular events. However, serial changes in plaque characteristics have not been reported in vivo. We evaluated the progression of coronary atherosclerosis in patients with T2DM using an integrated backscatter intravascular ultrasound (IB-IVUS) examination. Methods and results Forty-two T2DM and 48 non-diabetic patients who underwent percutaneous coronary intervention were enrolled in the study. Non-culprit 20-mm length coronary lesions with mild-to-moderate stenosis were measured using a 40-MHz (motorized pullback of 0.5 mm/s) IVUS catheter. IVUS examinations were performed on one target lesion in each patient. Six months later, a follow-up IVUS examination was repeated in the same coronary segment imaged at the baseline examination. T2DM patients demonstrated a greater total plaque volume (TPV; 139 ± 53 vs. 114 ± 45 mm3, P = 0.02) and total lipid volume (TLV; 67 ± 26 vs. 55 ± 30 mm3, P = 0.039) at the baseline examination. The progression of TPV (8.6 ± 15.4 vs. −2.2 ± 16.0%, P < 0.01) and TLV (10.8 ± 28.8 vs. −2.5 ± 20.0%, P < 0.05) from the baseline was observed in T2DM patients, but not in non-diabetic patients. The increase in TLV was blunted in T2DM patients who achieved HbA1c levels of <6.5%. Conclusion Accelerated plaque progression with an increase in the lipid-rich component of non-culprit plaques was observed in T2DM, despite the use of standard medical treatment. Better glycaemic control ameliorated the worsening of plaque characteristics in T2DM.

Angiotensin-converting enzyme 2 (ACE2) generates angiotensin-(1–7) Ang-(1–7), a peptide highlighted as exerting a pivotal role in cardiovascular remodeling. Moreover, the ACE2Ang-(1–7)Mas axis directly activates endothelial nitric oxide (NO) synthase and NO generation in the heart. However, the role of ACE2 in cardiovascular remodeling induced by persistent inhibition of NO under chronic activation of the renin–angiotensin system (RAS) remains poorly understood.

The aim of this study was to investigate the relationship between late gadolinium enhancement (LGE) and the effect of cibenzoline (CBZ) on left ventricular (LV) diastolic function in hypertrophic cardiomyopathy (HCM) patients. Echocardiography before and after intravenous CBZ (1.4 mg/kg over 5 minutes) and magnetic resonance imaging (MRI) were performed in 22 consecutive patients with HCM [mean age: 65 ± 14 years, obstructive HCM: 14, nonobstructive HCM (HNCM): 8]. The extent of LGE (%LGE = LGE volume/total LV volume) was obtained by contrast-enhanced MRI using custom software. LGE was observed in 19 patients (mean %LGE = 5.1% ± 3.9%). The propagation velocity of LV early filling flow (Vp) increased significantly in patients with obstructive HCM (26 ± 7 to 36 ± 14 cm/s, P= 0.001) and nonobstructive HCM (25 ± 9 to 36 ± 16 cm/s, P= 0.007). A significant negative correlation was observed between the change in Vp and %LGE in patients with HCM (r= −0.542, P= 0.009). Less extensive myocardial fibrosis, as demonstrated by LGE on contrast-enhanced MRI, may predict the ability of CBZ to improve LV diastolic function in HCM.

The renin–angiotensin system affects insulin sensitivity mainly through the angiotensin II type 1 receptor. In this study, the effects of renin inhibition on insulin resistance and adipose tissue dysfunction were explored in type 2 diabetic KK-Aymice.

We examined the possibility that activation of the human brain renin–angiotensin system is involved in enhancement of ischemic brain damage using chimeric transgenic mice with human renin (hRN) and human angiotensinogen (hANG) genes.

It was recently suggested that insulin resistance is significantly correlated with activation of the cardiac sympathetic nervous system in patients with essential hypertension.

The bis(1-methylimidazole)iron(II) complexes of porphyrins substituted with one, two, or four CF3groups at pyrrole ß-positions of a porphyrin have been studied by electronic absorption and magnetic circular dichroism (MCD) spectroscopies. The splittings of Q-bands observed in the electronic spectra of the complexes may arise from asymmetrical electronic effects of the highly electron-withdrawing CF3group on the porphyrin periphery. The ratio of absorption intensity (e(a)/(e(ß)) decreased with an increase of the number of CF3group, suggesting the decrease of a splitting in HOMOs. The MCD spectra of the bis(1-methylimidazole)iron(II) porphyrin complexes were markedly sensitive to the porphyrin peripheral substituents. The MCD spectra in Soret region successively changed in shape with the number of CF3group on porphyrin periphery and consequently were apparently inverted in sign, which can be explained by the shift of maximal wavelength accompanied by a change in intensity.

Supplemental Digital Content is available in the text.

Introduction:Slow/no-reflow phenomenon is a critical complication during PCI that leads to poor outcomes. Distal embolization is a known major contributing factor of slow/no-reflow phenomenon. Further, mechanical obstruction could cause slow/no-reflow phenomenon but its mechanism has not been fully investigated.Objectives:We examined mechanisms of slow/no-reflow phenomenon during percutaneous coronary intervention (PCI) using intravascular ultrasound (IVUS).Methods:We retrospectively analyzed IVUS data from 62 lesions in 58 consecutive patients [32 with ST-segment elevation myocardial infarction, 13 with non-ST-segment elevation acute coronary syndrome, and 13 with stable angina] who developed slow/no-reflow phenomenon during PCI. IVUS was performed immediately after the development of slow/no-reflow phenomenon to assess its cause. No mechanical obstruction by IVUS was categorized as distal embolization.Results:The results are summarized in the Figure. Distal embolization was observed in 46 lesions (74%). Of these lesions, most of the slow/no-reflow phenomenon occurred after stent implantation (45 lesions, 98%), and in-stent plaque protrusion was observed in 38 lesions (84%). In addition to distal embolization, 3 different mechanisms of slow/no-reflow phenomenon induced by mechanical obstructions (16 lesions, 26%) were clarified by IVUS. They were classified as dissection/hematoma (6 lesions), intimal flap (6 lesions), and thrombus obstruction (4 lesions). Most mechanical obstructions (13 lesions, 81%) could not be differentiated by angiography alone. In 15/16 lesions (94%) with mechanical obstruction, deteriorated flow improved immediately after balloon dilatation or bail-out stent implantation.Conclusions:The frequency of mechanical obstruction as the cause of the slow/no-reflow phenomenon was relatively high. IVUS assessment may provide reliable information for slow/no-reflow phenomenon management during PCI.

Supplemental Digital Content is available in the text.

Slow/no-reflow phenomenon during emergent percutaneous coronary intervention in patients with ST-elevation myocardial infarction (STEMI) results in a poor prognosis. A high thrombus burden was an independent predictor of angiographic slow/no-reflow phenomenon. We experienced a case of a STEMI patient with massive intracoronary thrombus. In our case, a massive red thrombus was aspirated easily by adjunctive pulse infusion thrombolysis (PIT) after failed aspiration. Adjunctive pulse infusion thrombolysis after failed aspiration might be a useful strategy to prevent the slow/no-reflow phenomenon in STEMI patients with massive intracoronary thrombus.

Aims Late gadolinium enhancement (LGE) on contrast-enhanced magnetic resonance imaging (MRI) in hypertrophic cardiomyopathy (HCM) has been reported to be associated with myocardial fibrosis and cardiac events. In patients with HCM, two-dimensional (2D) strain can identify subclinical global systolic dysfunction despite normal left ventricular (LV) chamber function. Therefore, this study tested the hypothesis that global 2D strain could detect subtle myocardial fibrosis and serve as a novel prognostic parameter in HCM patients. Methods and results Echocardiography and MRI were performed in 48 consecutive patients with HCM and normal chamber function. We measured global longitudinal strain (GLS) in apical two-chamber, four-chamber, and long-axis views using speckle-tracking analysis. The extent of LGE (%LGE = LGE volume/total LV volume) and LV mass index were calculated by MRI using Simpsons rule and custom software. All patients were followed up for major cardiac events. Global longitudinal strain in patients with LGE was significantly lower than that without LGE (−11.8 ± 2.8 vs. −15.0 ± 1.7%, P < 0.001). Multivariate analysis showed that GLS was an independent predictor of %LGE (standard coefficient = 0.627, P < 0.001). During a mean follow-up period of 42 ± 12 months, five patients had cardiac events. When the patients were stratified based on the median level of GLS (−12.9%), all events were observed in the worse GLS group (P = 0.018). Conclusion These results suggest that global 2D strain might provide useful information on myocardial fibrosis and cardiac events in HCM patients with normal chamber function.