A case of syncope after exertion due to sigmoid septum evaluated by exercise stress echocardiography.

A sigmoid septum is associated with sharp angulation and aging of the aortic root; however, it does not affect the pressure gradient in the left ventricular outflow tract and is generally asymptomatic. This report describes a 73-year-old woman who presented with syncope after exertion. Echocardiography revealed that the cause was left ventricular outflow tract stenosis associated with a sigmoid septum; her symptoms improved with beta-blocker therapy. Exercise stress echocardiography was performed to determine treatment efficacy. Sigmoid septum causes syncope on exertion; however, drug therapy is effective. Exercise stress echocardiography is effective in determining treatment efficacy. If syncope is present, a sigmoid septum should be considered as a cause. Learning objectives: 1.A sigmoid septum is part of or resembles hypertrophic cardiomyopathy, resulting in left ventricular outflow tract (LVOT) stenosis that is exacerbated by exertion and may cause syncope.2.A sigmoid septum is a differential diagnosis for the cause of syncope and is diagnosed using cardiac echocardiography.3.LVOT stenosis due to a sigmoid septum can be improved with drug therapy such as beta-blockers.4.The effects of beta-blocker therapy can be determined by exercise stress echocardiography.

Serum zinc concentration in patients with myocardial infarction: a retrospective study.

BACKGROUND: Zinc regulates the oxidative stress and inflammatory signaling cascade and affects the development and deterioration of cardiovascular disease. We investigated the prognosis of developing heart failure in patients with myocardial infarction. METHODS: Patients with myocardial infarction (n = 243) were divided using the median value of zinc concentration on admission into low (< 66 µg/dL at admission, n = 111) and high zinc group (≥ 66 µg/dL at admission, n = 132). During follow-up (mean ± SD: 734 ± 597 days; median 691 days), admission due to heart failure was observed in 12 patients: 10 and 2 cases in the low and high zinc groups, respectively. RESULTS: The risk of admission due to heart failure was significantly higher in the low zinc than in the high zinc group (P = 0.0043). Relative to the high zinc group, the hazard ratio for admission due to heart failure was 15.7 (95% confidence interval 1.11-221, P = 0.042) via adjusted Cox proportional hazards analysis. Even after propensity score matching, the risk of admission due to heart failure was significantly higher in the low zinc than in the high zinc group (P = 0.048). CONCLUSION: Low serum zinc concentration may be a risk factor for admission due to heart failure after myocardial infarction.

Effect of constipation on readmission for heart failure in patients with acute heart failure.

AIMS: Constipation is a common gastrointestinal disorder that is associated with a high cardiovascular event rate in the general population. Although constipation is common in patients with cardiovascular diseases, only a few studies have examined the relationship between constipation and the prognosis of patients with heart failure. This study aimed to evaluate the effects of constipation on the prognosis of patients with acute heart failure. METHODS AND RESULTS: We investigated 397 patients admitted to our hospital from December 2020 to December 2022 with acute heart failure (mean age, 81 ± 13 years; 54% men). Patients with constipation were defined as those either taking laxatives regularly or diagnosed with constipation according to the International Statistical Classification of Diseases and Related Health Problems. During the follow-up periods (median, 173 days), 35 patients died, and 74 experienced readmission due to heart failure. Kaplan-Meier analysis before and after propensity score matching using 14 variables revealed that the risk of readmission due to heart failure was significantly higher in patients with constipation than in those without (before: log-rank P = 0.014, after: log-rank P = 0.0027). The adjusted Cox proportional hazards analysis revealed that the hazard ratio for readmission due to heart failure was 2.61 (95% confidence interval, 1.38-4.94, P = 0.0032). The risk of all-cause death was not significantly different between the two groups (hazard ratio, 1.76; 95% confidence interval, 0.61-5.06; P = 0.30). CONCLUSIONS: Constipation status was strongly associated with a higher risk of readmission for heart failure in patients with acute heart failure.

Higher Recurrence Rate of Acute Coronary Syndrome in Patients with Multiple-Time Myocardial Infarction.

The recurrence rate of acute coronary syndrome (ACS) in patients after first-time myocardial infarction (MI) is over ten times higher than in the general population. However, it is unclear whether patients with multiple-time MI have an even higher recurrence rate of MI. This study aimed to compare the recurrence rate in patients with multiple-time MI with the rate in patients after first-time MI. We retrospectively studied 794 consecutive MI patients who were discharged. Recurrent ACS was investigated in patients with previous MI (n = 46) and without previous MI (n = 748). During the follow-up periods (mean ± SD: 757 ± 733 days), recurrent ACS occurred in 47 cases without previous MI and in 7 cases with previous MI. Kaplan-Meier analysis revealed that the risk of recurrent ACS was significantly higher in patients with previous MI than in patients without previous MI. ACS recurrence rates one year from the onset were 4.2% in patients without previous MI and 11.9% in patients with previous MI. Landmark analysis revealed that the higher recurrence rate in patients with previous MI was as high as 14.1% from 1 year after the onset to 2 years. In conclusion, the risk of recurrent ACS may be significantly higher in patients with multiple-time MI than in patients after first-time MI.

Irreversible deterioration of estimated glomerular filtration rate in patients with acute myocardial infarction after primary percutaneous coronary intervention.

Contrast-induced nephropathy is a possible complication after primary percutaneous coronary intervention (PCI) for acute myocardial infarction (MI). Deterioration of renal function is reported to be generally reversible. However, renal insufficiency worsens the prognosis for some patients with primary PCI. We evaluated sequential changes in renal function before primary PCI and until the chronic phase. We retrospectively studied 302 patients who had undergone PCI for acute MI. Renal function was evaluated based on estimated glomerular filtration rates (eGFRs) measured at the following four points: before PCI, within 1 week after PCI, at discharge from the hospital, and 180-365 days after MI. Patients were classified into the preserved eGFR group and the reduced eGFR group according to the median eGFR change from the basal level after PCI. Changes in eGFR in the two groups had significantly different time courses. In the preserved eGFR group, eGFR values during the chronic phase did not differ from the values obtained before PCI. In contrast, eGFRs in the reduced eGFR group did not recover to pre-PCI basal levels, with the median decrease being 10.3 mL/min/1.73 m2. The eGFR change after PCI was the strongest predictor of eGFR change during the chronic phase. In the reduced eGFR group, incidence of major adverse cardiac events was significantly higher (logrank: p = 0.048), and the hazard ratio was 2.28 (95 % confidence interval 1.02-5.60). A decline in eGFR after primary PCI for acute MI is not uncommon, and it appears to remain irreversible, even during the chronic phase.

A simple and rapid method for identification of lesions at high risk for the no-reflow phenomenon immediately before elective coronary stent implantation.

We aimed to design a rapid and reliable method to identify coronary lesions at high risk for the no-reflow phenomenon before elective coronary stent implantation using integrated backscatter intravascular ultrasound (IB-IVUS). The no-reflow phenomenon occurring during elective percutaneous coronary intervention (PCI) worsens patient prognosis, regardless of whether the phenomenon is transient or persistent. We retrospectively studied 353 coronary lesions to identify factors potentially promoting the no-reflow phenomenon, including lesion location and severity. We also performed component analysis by two- and three-dimensional IB-IVUS before elective stent implantation. The cutoff values of the true lipid volume and estimated lipid volume (lipid area at the minimal lumen diameter site × total stent length) for the no-reflow phenomenon were determined by receiver operating curve analysis. Type C lesions, regardless of location and a thrombolysis in myocardial flow grade of 0, were risk factors for the no-reflow phenomenon during PCI. The estimated lipid volume was significantly correlated with the true lipid volume (R 2 = 0.778, p < 0.0001). The cutoff value of the estimated lipid volume for the no-reflow phenomenon was 132.6 mm3 (area under the curve = 0.719), and the predictive value was equivalent to that of the true lipid volume. Lesions with an estimated lipid volume of ≥132.6 mm3 had a significantly higher risk of the no-reflow phenomenon during elective stent implantation (odds ratio, 4.35; 95 % confidence interval, 1.67-12.7; p = 0.0024). The simple and rapid measurement of the estimated lipid volume immediately before stenting during PCI constitutes a reliable predictor of lesions at high risk for the no-reflow phenomenon.

The systemic inflammation-based Glasgow Prognostic Score as a prognostic factor in patients with acute heart failure.

AIMS: By combining C-reactive protein and serum albumin concentrations, the Glasgow Prognostic Score (GPS) provides valuable predictions of prognosis in patients with cancer. Both systemic inflammatory response and malnutrition are also common in patients with heart failure. We evaluated the efficacy of the GPS for predicting the prognoses of patients with acute decompensated heart failure (ADHF). METHODS: We investigated 336 patients who were admitted with ADHF. The GPS (0, 1, and 2) was defined as follows: patients with both elevated C-reactive protein (>1.0 mg/dl) and hypoalbuminemia (<3.5 g/dl) were allocated a score of 2, patients with only one of these biochemical abnormalities were allocated a score of 1, and patients with neither of these abnormalities were allocated a score of 0. RESULTS: During the follow-up period (mean ±â€ŠSD: 504 ±â€Š471 days), 71 patients (21.1%) died. Relative to a GPS of 0, the hazard ratios for all-cause death were 3.40 (95% confidence interval 1.81-6.45) for a GPS of 2 and 1.97 (95% confidence interval 1.06-3.66) for a GPS of 1, as determined using adjusted Cox proportional-hazards analysis. CONCLUSIONS: The GPS, which is based on systemic inflammation, is useful for predicting the prognoses of hospitalized patients with ADHF.

High serum erythropoietin level is associated with smaller infarct size in patients with acute myocardial infarction who undergo successful primary percutaneous coronary intervention.

OBJECTIVES: We investigated whether a higher serum erythropoietin (EPO) level in patients with acute myocardial infarction (MI) subjected to successful primary percutaneous coronary intervention (PCI) can predict a smaller infarct size determined by creatine kinase (CK) release. BACKGROUND: Erythropoietin has been shown to protect cardiomyocytes from ischemia-reperfusion injury in rodents. METHODS: We prospectively studied 101 patients with first MI who received successful primary PCI within 12 h from the onset of MI. Blood samples were collected to examine the serum EPO level after the primary PCI and within 24 h from the onset of MI. RESULTS: The peak CK level and cumulative CK release were significantly lower in the above-median EPO group than in the below-median EPO group. Thrombolysis In Myocardial Infarction (TIMI) grades and collateral grades before PCI, infarct-related coronary arteries, time to the successful reperfusion from the onset of MI, and serum creatinine levels were similar in the two EPO groups. A stepwise multiple regression analysis revealed that the absolute serum EPO level (mU/ml) as well as TIMI grades after PCI and preinfarction angina was an independent predictor for the cumulative CK release. CONCLUSIONS: These data suggest that a high endogenous EPO level can predict a smaller infarct size in patients with acute MI subjected to successful primary PCI. This might be attributed to the potentially protective effect of endogenous EPO against ischemia-reperfusion injury in humans.

Myocardial 11C-diacylglycerol accumulation and left ventricular remodeling in patients after myocardial infarction.

UNLABELLED: Left ventricular (LV) remodeling after myocardial infarction (MI) is a maladaptive process that increases the risk of heart failure and death. The myocardial phosphoinositide cycle, which is located downstream from several neurohumoral factors, plays a crucial role in LV remodeling. Our animal studies demonstrated that 1-[1-11C]butyryl-2-palmitoyl-rac-glycerol (11C-DAG) can be used to visualize regions with an activated phosphoinositide cycle. Therefore, we examined whether myocardial 11C-DAG accumulation assessed by PET is relevant to LV enlargement and systolic dysfunction in post-MI patients. METHODS: We performed PET with 11C-DAG in 13 post-anteroseptal MI patients and 4 healthy volunteers. We placed regions of interest on the noninfarcted myocardium and calculated the myocardium-to-left atrial (LA) chamber ratio of 11C-DAG accumulation. RESULTS: The myocardium-to-LA chamber ratio of 11C-DAG was significantly higher in the post-MI patients (mean +/- SD, 1.73 +/- 0.35) compared with that of the healthy volunteers (mean +/- SD, 1.25 +/- 0.13; P < 0.05). In the post-MI patients, the myocardium-to-LA chamber ratio of (11)C-DAG was significantly correlated with the LV end-diastolic volume index (r = 0.79, P < 0.01) and the plasma concentration of brain natriuretic peptide (r = 0.85, P < 0.001) and negatively correlated with the LV ejection fraction (r = -0.69, P < 0.01). CONCLUSION: These findings suggest that the myocardial 11C-DAG accumulation assessed by PET is relevant to LV enlargement, LV systolic dysfunction, and humoral activation in post-MI patients. This new imaging strategy based on intracellular signaling may contribute to the assessment and treatment of post-MI patients.

Effect of angiotensin converting enzyme inhibition on myocardial phosphoinositide metabolism visualised with 1-[1-11C]-butyryl-2-palmitoyl-rac-glycerol in myocardial infarction in the rat.

We recently reported that myocardial phosphoinositide (PI) metabolism can be visualised by 1-[1-11C]-butyryl-2-palmitoyl-rac-glycerol (11C-DAG) in rats with myocardial infarction (MI). Angiotensin II, the receptors for which are expressed predominantly in infarcted areas with active fibrogenesis rather than in non-infarcted regions, is involved in the upstream signalling systems of PI metabolism and plays an important role in the process of left ventricular (LV) remodelling after MI. We therefore hypothesised that the distribution of 11C-DAG after MI may be affected by the inhibition of angiotensin converting enzyme, which is one of the most important factors in the development of LV remodelling after MI. Rats were injected with 11C-DAG after 3 or 10 weeks of treatment with captopril or no treatment following coronary artery ligation, and quantitative autoradiography was performed. Cells occupying the infarcted region were identified by immunohistochemistry. Compared with untreated rats, treatment with captopril for 3 weeks after MI elicited a reduction in the 11C-DAG uptake in the infarcted region (P<0.05) but not in the non-infarcted region, and was associated with a 22% decrease in the heart weight/body weight ratio. The thallium-201 distribution in the infarcted area was similarly low in the rats with and rats without the 3-week captopril treatment after MI. Abundant macrophages and myofibroblasts occupied the infarcted area in both rats with and rats without the captopril treatment for 3 weeks after MI. The 11C-DAG radioactivity in the infarcted region in the untreated rats was lower 10 weeks after MI than 3 weeks after MI (P<0.01). This finding was in agreement with the results of immunohistochemistry demonstrating that the number and size of macrophages and myofibroblasts were remarkably reduced in rats 10 weeks after MI compared with 3 weeks after MI. Captopril treatment for 10 weeks after MI did not decrease the 11C-DAG radioactivity in the infarcted area further. These data suggest that 11C-DAG is useful for visually detecting regions with activated PI metabolism after MI, and that captopril reduces PI metabolism in the infarcted region in the relatively early phase of MI, which might contribute to the attenuation of ventricular remodelling.