BACKGROUND:Delayed heart rate (HR) and blood pressure recovery after exercise test is known as the reliable indexes of autonomic dysfunction. Here we tried to evaluate the serial changes in various indicators during exercise test and correlations with recovery of HR and blood pressure in a normotensive healthy middle-aged group.METHODS:A total of 122 patients without hypertension or diabetes was enrolled (mean age, 55.6 ± 11.0; male, 56.6%; mean blood pressure, 124.8 ± 16.6 / 81.5 ± 9.6 mmHg). Treadmill test was performed for evaluation of chest pain. Patients with coronary artery disease, positive treadmill test result, left ventricular dysfunction or renal failure were excluded. Heart rate recovery was calculated by subtracting the HR in the first or second minute of recovery period from the HR of peak exercise (HRR1 or HRR2). Systolic blood pressure in the 4th minute of recovery stage (SBPR4) was used to show delayed blood pressure recovery.RESULTS:Metabolic equivalents (METs) and HR in stage 2 to 4 were significantly correlated with both HRR1 and HRR2. Multiple regression analysis of HRR revealed significant correlation of METs and SBPR4. SBPR4 was significantly correlated with both HRR1 and HRR2 (HRR1, r = -0.376, p<0.001; HRR2, r = -0.244, p = 0.008) as well as SBP in the baseline to stage 3 and pulse pressure (r = 0.406, p<0.001).CONCLUSIONS:Delayed BP recovery after peak exercise test revealed significant association with autonomic dysfunction and increased pulse pressure in normotensive middle-aged healthy group. It can be a simple and useful marker of autonomic dysfunction and arterial stiffness.

https://e-jcvi.org As is well known, the left atrium (LA) is usually thought of as a way to supply blood flow to the left ventricle (LV) (the conduit function) as well as a place to store blood (the reservoir function); however, the LA also satisfies an important active pumping role in filling the ventricles with blood (the booster pump function). The principal function of the LA is to modulate LV filling and cardiovascular performance. The atrial booster pump function reflects the magnitude and timing of atrial contractility, but is dependent on the degree of venous return (atrial pre-load), LV end-diastolic pressures (atrial afterload), and LV systolic reserve.1)

Background Fundamental echocardiography has some drawbacks in patients with difficult-to-image echocardiograms. The aim of this study is to evaluate impact of contrast echocardiography (CE) on ventricular function assessment and clinical diagnosis in routine clinical echocardiography. Methods Two hundred sixty patients were prospectively enrolled over 3 years in 12 medical centers in Korea. General image quality, the number of distinguishable segments, ability to assess regional wall motion, left ventricular (LV) apex and right ventricle (RV) visualization, LV ejection fraction, changes in diagnostic or treatment plan were documented after echocardiography with and without ultrasound contrast agent. Results Poor or uninterpretable general image was 31% before contrast use, and decreased to 2% (p<0.05) after contrast use. The average number of visualized LV segments was 9.53 before contrast use, and increased to 14.46 (p<0.001) after contrast use. The percentage of poor or not seen LV regional wall motion was decreased from 28.4% to 3.5% (p<0.001). The percentage of poor or not seen LV apex and RV was decreased from 49.4% to 2.4% (p<0.001), from 30.5% to 10.5% (p<0.001), respectively. Changes in diagnostic procedure and treatment plan after CE were 30% and 29.6%, respectively. Conclusion Compared to fundamental echocardiography, CE impacted LV function assessment and clinical decision making in Korean patients who undergo routine echocardiography.

A 73-year-old man with uncontrolled nocturnal hypertension presented to the hospital for postural hypotension.He presented with a past history of cerebral infarction, parkinsonism, transient ischemic attack, and chronic renal failure.An electrocardiogram, chest X-ray, and laboratory test revealed normal findings.Ambulatory blood pressure (BP) monitoring was performed for 24 hours to evaluate his pattern of BP revealing a day-time average BP of 136/82 mmHg and night-time average BP of 190/106 mmHg (Fig. 1A).A transthoracic echocardiography showed normal heart functioning; however, an interesting Doppler pattern in the left ventricular outflow tract (LVOT), according to each posture, was found.Greater decreased velocity-time integrals in a standing position were noted than when in a sitting or supine position with significantly decreased blood pressure (Fig. 1B-D).Orthostatic hypotension is not a rare symptom in the general population.Impaired autonomic reflexes can lead to a significant reduction in BP upon standing.The impairment results from deficits in hemodynamic responses, including inadequate ventricular filling, excessive decreases in cardiac output or venous return, and failure of the skeletal muscle pump to increase venous return to the heart. 1-3) We evaluated the Doppler at LVOT according to each posture in one patient and it presented an interesting Doppler pattern immediately after a postural change.A doppler image can present typical and characteristic hemodynamic changes of stroke volume in orthostatic hypotension.To the best of our knowledge, this is the first report showing the decreasing stroke volume in orthostatic hypotension through various position changes in one patient.

There are many studies that show the myocardial fibrosis resulting from hypertension, aortic stenosis or hypertrophic cardiomyopathy, which are under the same condition with chronic pressure overloading. Multiple factors are recommended for impaired cardiac function in patients with hypertension, such as inflammation, adaptive ventricular remodeling, increased mechanical stress inducing subsequent ventricular hypertrophy, interstitial and perivascular fibrosis, endothelial dysfunction and neurohormonal factors. The development of left ventricular (LV) hypertrophy is actually a combined consequence of chronic pressure or volume overload in hypertension or aortic stenosis. To compensate for chronic pressure overload in these subjects, LV wall thickness gradually increases in order to normalize wall stress, leading to concentric LV remodeling and hypertrophy. Activation of several biological processes including various hormones, growth factors and cytokines also contribute to protein genesis by promoting muscle cell growth, leading to structural alterations and remodeling. We can inference the fatigue and essential compensatory mechanism of myocardium. The similar process can occur in obese patients. Moderate to severe cases of obesity was presented as leading to increased LV wall stress, compensatory LV hypertrophy and LV dysfunction. Alpert used a term of ‘obesity cardiomyopathy’ expressing the series of myocardial dysfunction. Compared with healthy lean individuals, increased epicardial adipose tissue in obese group is expected to result in more extensive fatty infiltration in the myocardium. They showed the correlation between incidence of atrial fibrillation and an excess adiposity and fibrosis in obesity with histologic demonstration. pISSN 1975-4612/ eISSN 2005-9655 Copyright © 2016 Korean Society of Echocardiography www.kse-jcu.org https://doi.org/10.4250/jcu.2016.24.4.274

BACKGROUND:Pregnancy induces dramatic cardiovascular changes in order to meet the increasing metabolic needs. Adaptive change of left ventricle (LV) might be modified in pregnancy complicated by hypertension.METHODS:Data from 193 consecutive pregnant women were analyzed. Clinical and echocardiographic data were compared in normotensive and hypertensive women.RESULTS:Significantly higher LV mass indexed by height was observed in hypertensive women compared with normotensive women (84 ± 21 g/m vs. 97 ± 20 g/m, p = 0.001). Diastolic function measured by the ratio of peak velocity of early diastolic transmitral blood flow to early diastolic mitral annular velocity was impaired in hypertensive women (11.0 ± 3.0 vs. 9.2 ± 2.5, p < 0.001). Such change was more prominent in women with gestational hypertension (GH) than those with chronic hypertension (CH). Heavy maternal weight was an independent factor associated with LV hypertrophy (LVH) in both normotensive and hypertensive women. Overt eccentric LVH was more frequent than concentric remodeling/hypertrophy (24% vs. 8.4%) in GH, while the opposite result was observed in CH (14% vs. 23%).CONCLUSION:Hypertensive pregnancy is associated with significant LVH and diastolic dysfunction. CH seems to induce different LV remodeling pattern from GH. Heavy maternal weight during pregnancy might intensify the unfavorable remodeling of LV, particularly in hypertensive pregnancy.

Aneurysms of the left main coronary artery are very rare in patients with acute coronary syndrome.The increased accuracy of computed tomography permits the detection of coronary artery anatomic structures after one peripheral injection of contrast agent.We report a 42-year-old man with a left main coronary aneurysm, with a thrombus presenting as non-ST elevation myocardial infarction, detected by coronary computed tomographic angiography.(

A huge thumb in the heartA 69-year-old woman with hypertension, with dyspnoea for 1 month, was admitted to the emergency department.On presentation, transthoracic echocardiography showed preserved left ventricular systolic function (ejection fraction=52%) and a large, highly mobile linear cystic mass in the right atrium coming from the inferior vena cava (figure 1A,B, arrowheads; online supplementary videos 1-3).Severe tricuspid stenosis was shown during the diastolic phase owing to a large mobile mass in the right ventricular inflow portion (Vmax=1.6 m/s, peak/ mean diastolic pressure gradient=10/6 mm Hg).Abdominal CT showed a heterogeneous large mass in the left kidney and heterogeneous internal low density in the left renal vein, inferior vena cava and right atrium, suggestive of renal cell carcinoma and tumour thrombosis (figure 1C-E, arrowheads).She refused surgery and is being treated with chemotherapy for the renal cell carcinoma and anticoagulation for thrombi in the heart.

Coronary artery fistulas have been diagnosed with aortography, coronary angiography, and coronary computed tomography (CT). A large fistula can be occasionally found as a mass lesion on echocardiography but cannot be easily confirmed. Here, we report a new diagnostic approach to coronary artery fistulas using a contrast agent and transthoracic echocardiography. Transthoracic echocardiography of a 46-year-old female suffering from dyspnea revealed suspicious small turbulent flow in the main pulmonary artery. Following infusion of a contrast agent, we found whitish flow in the main pulmonary artery during the diastolic phase, and aortic CT revealed two huge right coronary artery fistulas in the main pulmonary artery. A simple diagnostic approach to a coronary artery fistula using contrast agent helped us confirm the diagnosis because of the typical diastolic whitish flow in the pulmonary artery.

BACKGROUND:The effect of gestational hypertension on left ventricular (LV) function in previously normotensive young women has not been evaluated.METHODS AND RESULTS:A total of 106 gestational hypertensive women (GHW, 32.3 ± 4.2 years) and 93 normotensive pregnant women (NPW, 30.2 ± 4.4 years) were enrolled. Transthoracic echocardiography, including 2-dimensional strain echocardiography, was done and myocardial performance (Tei index), LV mass index (LVMI), and relative wall thickness (RWT) were analyzed. GHW had significantly increased wall thickness (interventricular septum, 9.5 ± 0.9 mm vs. 8.8 ± 1.0 mm, P < 0.001; posterior wall, 9.0 ± 1.1 mm vs. 8.5 ± 1.1 mm, P = 0.007; and RWT, 0.39 ± 0.06 vs. 0.35 ± 0.05, P = 0.02), higher LVMI (95.6 ± 17.3g/m² vs. 86.1 ± 14.5g/m², P = 0.03), longer isovolumetric relaxation time (117.7 ± 18.2 ms vs. 82.3 ± 12.6 ms, P = 0.003), lower E/A ratio (1.00 ± 0.29 vs. 1.27 ± 0.33, P = 0.002), and higher Tei index (0.48 ± 0.23 vs. 0.33 ± 0.13, P = 0.003) compared to NPW. Global longitudinal LV strain, representing LV systolic function, was also significantly reduced in GHW compared with NPW (-17.6 ± 2.95% vs. -21.2 ± 2.14%, P = 0.02). A total of 62% of GHW (n = 66) had abnormal geometry, of whom, 42 (40%) had eccentric hypertrophy (EH). A total of 93% of NPW (n = 86) had normal geometry, and only 7 NPW (7%) had abnormal geometry.CONCLUSIONS:GHW had aggravated diastolic and longitudinal systolic dysfunction. GHW had increased LVMI with the abnormal geometric pattern of EH. The reversibility of these morphological and functional impairments after delivery needs to be clarified.

BACKGROUND Statins and angiotensin receptor blockers (ARBs) are known to improve vascular dysfunction in patients with chronic kidney disease. However, these effects have been inconsistent in dialysis patients. Moreover, it is currently unknown whether adding statins to ARBs improves vascular dysfunction better than ARB monotherapy in these patients. METHODS We conducted a prospective open randomized trial to investigate the effects of statin add-on to ARB on vascular protection in 124 nondiabetic patients undergoing peritoneal dialysis (PD). Initially, all patients received 80 mg/day of valsartan for 6 months. Excluding 10 patients who dropped out during this period, patients were randomly assigned to continue ARB treatment alone (n = 57) or to receive 10 mg/day of rosuvastatin (n = 57) added to ARB for the next 6 months. To assess vascular function, endothelium-dependent vasodilation and arterial stiffness were determined by brachial artery flow-mediated dilation (FMD) and brachial-ankle pulse wave velocity (baPWV), respectively. RESULTS Compared to baseline values, ARB treatment for the first 6 months significantly improved FMD% (2.97 ± 2.64 to 3.57 ± 2.58 %, P < 0.001). In addition, there was a small but significant decrease in baPWV during this period (1691.5 ± 276.3 to 1635.0 ± 278.6 cm/s, P = 0.048). After randomization, add-on treatment further improved FMD% (3.57 ± 2.73 to 4.24 ± 2.77 %, P = 0.003), whereas ARB monotherapy did not (P = 0.02 for between-group difference). Further slight improvement in baPWV (1617.0 ± 280.9 to 1528.9 ± 266.8 cm/s, P = 0.021) was observed only in the combined treatment group (P = 0.28 for between-group difference). CONCLUSIONS Adding a statin to the ARB was of some help in improving vascular dysfunction more effectively than ARB monotherapy in nondiabetic PD patients. However, whether such limited improvements can lead to better clinical outcomes requires further investigation.

RAGE is pattern recognizing receptors for diverse endogenous ligands. RAGE activation by RAGE ligands is known to be associated with reactive oxygen species generation, activation of NF kappa B, as well as recruitment of proinflammatory cells. Activated endothelial cells, vascular smooth muscle cells in atherosclerotic plaques and activated inflammatory cells all have increased expression of RAGE, which with its interaction with RAGE ligands increases the secretion of proinflammatory cytokines and cell adhesion molecules. Furthermore, RAGE may have a significant role in leukocyte recruitment into the intima of the atherosclerosis. Initial insults resulting in endothelial dysfunction will result in leukocyte infiltration, oxidative stress and vascular inflammation that is amplified by RAGE activation. RAGE and its interaction with RAGE ligands may be important for initializing and maintaining the pathological processes that result in various entities of cardiovascular disease. Soluble RAGE competitively inhibits the binding of RAGE ligands to RAGE and attenuates the development of atherosclerosis in vivo. Thus RAGE may be a promising target for treatment of cardiovascular disease in the future.

The percutaneous transfemoral approach has been routinely used for cardiac catheterization and coronary angioplasty. Local vascular complications following angioplasty are seen in 5% to 10% of patients, especially in those who need prolonged anticoagulation. Transradial access for coronary procedures dramatically reduces access site complications. We report a rare case of radial arteriovenous fistula, which developed after coronary angiography perfomed using the transradial approach.

This study aimed to investigate the factors determining early left atrial (LA) reverse remodeling after mitral valve (MV) surgery. The left atrium is frequently dilated in patients with mitral stenosis (MS) or mitral regurgitation (MR). MV surgery usually results in LA volume reduction. However, the factors associated with LA reverse remodeling after MV surgery are not clearly defined. One hundred thirty-eight patients (51 men, 87 women; mean age, 53 years) underwent transthoracic echocardiography before and after MV surgery. Maximal LA volume was measured using the prolate ellipsoid model. The percentage of LA volume change was calculated. The patients were grouped according to age.(< 50 vs >= 50 years), predominant lesion (pure MR vs some degree of MS), type of surgery (MV repair vs MV replacement), and preoperative rhythm (sinus rhythm vs atrial fibrillation). LA volume decreased from 147 +/- 93 to 103 +/- 43 ml (p < 0.001) after surgery. LA reverse remodeling was more prominent in patients who were < 50 years old (percentage of LA volume change -31.2 +/- 17.4 vs -18.4 +/- 1.9.2, p < 0.001), had pure MR (percentage of LA volume change -30.4 +/- 18.6 vs -17.3 +/- 18.2, p < 0.001), and had a preoperative sinus rhythm (percentage of LA volume change -28.5 +/- 17.7 vs -20.5 +/- 20.0, p = 0.019). In conclusion, on stepwise multiple regression analysis, preoperative LA volume, predominant lesion, age, and cardiac rhythm were significant predictors of LA reverse remodeling. A larger preoperative LA volume, MR rather than MS, younger age at the time of surgery, and sinus rhythm were important predictors of LA reverse remodeling after MV surgery. (c) 2008 Elsevier Inc. All rights reserved.

Background: The pathophysiological role and metabolic pathway of Lp(a) have not been clearly defined. An association between Lp(a) and oxidative low-density lipoprotein (LDL) were recently reported. And small dense LDL (sd-LDL) were associated with circulating malondialdehyde-modified LDL. We investigated the relationships between serum Lp(a) level and LDL particle size in coronary artery disease (CAD) patients. Further, we investigated the relationships of sd-LDL and Lp(a) with the extent and severity of CAD. Methods: A total of 490 patients (mean: 60.5 ± 11.5 years old) who underwent coronary angiography to evaluate chest pain were investigated. Patients were classified into two groups, a CAD group (n = 256), who had significant stenosis observed by coronary angiogram, and a control group (n = 234), who had normal, or minimal coronary arteries. CAD severity was measured by Gensini scores. The distribution of the LDL subfraction was analyzed using a Quantimetrix Lipoprint LDL System. Results: The serum Lp(a) concentration was correlated with the fraction of sd-LDL (r = 0.193, p < 0.001) and mean LDL size (r = 0.160, p = 0.003). The Lp(a) level and mean LDL particle size were significantly correlated with a high Gensini score. LDL particle size in the CAD group was smaller than in the control group (26.74 ± 0.64 vs. 26.43 ± 0.93 nm, p < 0.001). The Gensini score was significantly higher in small LDL with high Lp(a) level groups. Conclusion: The positive correlation of the level of Lp(a) and sd-LDL fraction were demonstrated. The mechanism of this association is not clearly defined; we can suggest that it may stem from the individual atherogenic condition that linked to increased oxidative stress. Both increased Lp(a) and sd-LDL fraction were correlated with the severity of CAD.