Hajime Kataoka

Pericardial and pleural effusions in decompensated chronic heart failure

BACKGROUND In decompensated chronic heart failure, there is controversy regarding the incidence and amount of pericardial fluid. Moreover, the relation of pericardial effusion to pleural effusion has not yet been clarified. The current study examined the incidence and amount of pericardial effusion in patients with decompensated chronic heart failure as a function of the volume of pleural effusion. METHODS AND RESULTS The study subjects were 60 consecutive patients with chronic heart failure requiring diuresis to improve the symptoms and signs of congestion. Pericardial effusion was semiquantified on the basis of M-mode echocardiographic findings and the volume of thoracic effusion drawn from computed tomographic images of the chest with Simpsons method. Causes of decompensated chronic heart failure in the 60 patients included cardiac valve disease (n = 26), arterial hypertension (n = 12), chronic ischemic heart disease (n = 9), and others (n = 13). As many as 52 (87%) of the 60 patients had pleural effusion; of these, 45 had bilateral effusion, 5 had right-sided effusion only, and 2 had left-sided effusion only. In contrast, only 12 (20%) patients had small (n = 9) or moderate (n = 3) pericardial effusion. There was no significant association between the amount of pleural effusion and the semiquantified pericardial effusion (chi-square 3.27, P =.775). CONCLUSIONS In this series of patients with congestive heart failure, small pericardial effusion was sometimes observed, but moderate to large effusion was uncommon, and there was no significant association between a given amount of pleural effusion and the volume of pericardial effusion.

Electrocardiographic patterns of the Brugada syndrome in right ventricular infarction/ischemia

is not obese. Many athletes have physiques with minimal fat, but their BMIs are in the range that qualify for orlistat use. Second, the long-term effects of orlistat are not known. Orlistat leads to the malabsorption of vitamins A, D, E, and beta-carotene. Because it decreases all fat absorption by one third, it will decrease the absorption of omega-3 fatty acids, which have numerous health benefits.3 Orlistat should be selectively prescribed, case by case, based on BMI, physique, and other comorbidity. It would be wrong to prescribe this new drug to 100 million people based on an arbitrary and sometimes misleading number. That is far too many guinea pigs in an uncontrolled trial.

Hemostatic changes induced by percutaneous mitral valvuloplasty

A study was conducted of hemostatic changes in 15 patients with mild-to-moderate rheumatic mitral stenosis who underwent percutaneous mitral balloon valvuloplasty (PMV). The patients were divided into two groups according to the degree of valve dilatation as evaluated by Doppler echocardiography before and 2 to 3 months after therapy: one group (n = 7) with suboptimal valvuloplasty (< 0.5 cm2) and one (n = 8) with optimal valvuloplasty (> or = 0.5 cm2). On the day of echocardiographic evaluation, hemostatic testing of the platelet, coagulation, and fibrinolytic systems was performed. Before PMV there were no differences in the hemodynamic and hemostatic variables between the two groups. No favorable hemostatic changes were achieved by PMV in the suboptimal group. In the optimal group, however, platelet-specific protein levels decreased after PMV; the mean levels of platelet factor 4 and beta-thromboglobulin were moderately elevated before and decreased after PMV from 38.5 +/- 22.2 to 8.13 +/- 5.08 ng/ml (p < 0.01) and from 132.5 +/- 78.6 to 38.8 +/- 19.5 ng/ml (p < 0.02), respectively. Coagulation and fibrinolytic systems were unchanged in this study. These data indicate that PMV produces favorable hemostatic effects when sufficient mitral valve dilatation is achieved. Analysis of our data also discloses that platelet activation plays an important role in the initial step of thrombus formation in patients with rheumatic mitral stenosis.

Changes in the amplitude of electrocardiogram QRS complexes during follow-up of heart failure patients

INTRODUCTION Changes in the electrocardiogram QRS amplitudes (ECGΔ) during follow-up of heart failure (HF) patients have not been clinically exploited heretofore. METHODS We examined ECGΔ during follow-up of HF patients by employing 42 triplets of ECGs, other laboratory and HF-related clinical data corresponding to clinical stability, worsening, and recovery from 37 HF patients. RESULTS The % changes (Δ%) in the summed QRS amplitude of all 12 leads (ΣQRS(12L)), 6 precordial leads (ΣQRS(V1-V6)), 6 limb leads (ΣQRS(6L)), leads I+II (ΣQRS(I + II)), and lead aVR were evaluated. Also relationships between the ECG variables and body weight (BW), percent body-fat, and B-type natriuretic peptide (BNP) were examined. The QRS amplitude(s) in all ECG variables decreased from clinical stability to worsening HF, and returned to baseline at recovery. During HF worsening, Δ% was highest in lead aVR (-15.3 ± 12.3%), followed by Δ% in ΣQRS(6L) (-12.9 ± 10.1%) and ΣQRS(I + II) (-12.1 ± 10.8%). At worsening HF and its recovery, Δ% in ΣQRS(6L) correlated with Δ% in percent body-fat (r = 0.333, P = .031; r = 0.308, P = .047). At recovery, Δ% in each ECG variable correlated with Δ% in BW. Receiver operating characteristic (ROC) analysis showed that ≥16% reduction of ΣQRS(6L) and ΣQRS(I + II) discriminated between stable and worsening HF, with a sensitivity of 43% and 40%, and specificity of 98% for both. ECG variables from limb lead(s) had as good area under the curve (AUC) (0.78-0.84) as BNP (AUC: 0.88) for identifying worsening HF. CONCLUSIONS Changes of the QRS amplitudes in ECGs are as useful for monitoring HF patients as BNP.

ST Elevation in the right chest leads in anterior wall left ventricular acute myocardial infarction

Abstract Many studies 1,2 have reported the use of right chest leads for the evaluation of acute right ventricular (RV) infarction or proximal right coronary disease 2,3 in the presence of inferior wall left ventricular (LV) infarction. However, the characteristics of ST shift and the clinical usefulness of these leads in anterior wall LV acute myocardial infarction have been less fully evaluated. 4 Therefore, we compared the incidence, distribution and pattern of ST elevation in the right chest leads between the 2 conditions and assessed the clinical usefulness of these leads for evaluation of anterior wall LV acute myocardial infarction.

Short-term dynamic changes in hematologic and biochemical tests during follow-up of definite heart failure patients

There are few studies on the short-term changes in routine peripheral blood data in definite heart failure (HF) patients. This study examined whether or not such changes existed and evaluated the feasibility of monitoring changes in common blood tests to estimate body fluid status in HF patients. The blood test data both at worsening and recovery of HF status were obtained from 27 definite HF patients. Hemoglobin, hematocrit, total protein, albumin, and creatinine values were significantly lower during the period of worsening HF status than those obtained during a period of recent clinical stability. At recovery, the values of all measured blood markers had significantly increased compared to those obtained during the period of worsening HF status. At recovery, changes in body weight were negatively correlated with hemoglobin (r=-0.475, p=0.012), hematocrit (r=-0.429, p=0.026), and total protein (r=-0.442, p=0.021). Careful attention should be paid to short-term changes in routine blood tests to correctly interpret test results and to aid in monitoring body fluid status in HF patients.

Vascular expansion during worsening of heart failure: Effects on clinical features and its determinants ☆ ☆☆

BACKGROUND This study investigated the relation of the changes in serum solutes/albumin to the level of vascular expansion and clinical features during worsening HF. METHODS Data from 47 patients with acute on chronic HF worsening were analyzed. Blood tests included hemoglobin, hematocrit, albumin, solutes (Na/K/Cl/BUN/Cr), and b-type natriuretic peptide (BNP). The relative change in the vascular expansion from stable to worsening HF was estimated based on changes in the plasma volume (%PV). RESULTS When divided into two groups based on the median %PV, the clinical features of the expansion group (11≤%PV [range 11% to 36%]; n=24) included a lower incidence of crackles (13% vs. 52%, p=0.005) and a tendency toward preserved renal function (83% vs. 57%, p=0.06) compared with the non-expansion group (%PV [range -19% to 11%]<11; n=23), whereas the increase in body weight and log BNP did not differ between groups. The expansion group had a greater increase in serum Na (3.58±4.43 vs. -0.11±3.31mEq/L, p=0.0016) and Cl (5.54±6.24 vs. -0.03±4.18mEq/L, p=0.0006), and a decrease in serum albumin (-0.37±0.3 vs. -0.16±0.3g/dL, p=0.04) and creatinine (-0.28±0.39 vs. -0.06±0.22mg/dL, p=0.027) from stability to worsening HF. Multivariate logistic regression analysis revealed an independent association between the increase in %PV and the increase in the serum Cl concentration from stability to worsening HF (odds ratio: 12.2, 95% confidence interval: 1.78-83.8, p=0.011). CONCLUSIONS Though this study is observational and does not allow for causal inference, it may nonetheless be speculated that a greater accumulation of Cl in the blood vessels acts to increase or maintain intravascular volume, which induces different clinical features of HF.

Emergent coronary angiographic findings of patients with ST depression in the inferior or lateral leads, or both, during anterior wall acute myocardial infarction

In conclusion, the present study indicates that there are several distinctive differences in emergent coronary angiographic findings according to the presence or absence of ST depression in the inferior or lateral leads, or both, and location of the leads showing ST depression on admission electrocardiograms in patients with anterior AMI. The coronary angiographic features of patients with this ECG finding greatly support a poor prognosis. In patients with anterior AMI, analysis of ST depression on an admission electrocardiogram should be routinely performed because it is useful in predicting coronary anatomy, the extent of infarction, and its prognosis.

Exercise-induced precordial ST-segment depression in prior inferior myocardial infarction with single-vessel disease; with special reference to its mechanisms and distinction from multi-vessel disease

We investigated the mechanisms of exercise-induced precordial ST-segment depression on the electrocardiogram in prior inferior myocardial infarction with single-vessel disease and attempted to differentiate the ST-segment depression between single- and multi-vessel disease. Subjects included three groups: group Ia (n = 11), inferior myocardial infarction with single-vessel disease that showed no precordial ST-segment depression; group Ib (n = 7), inferior myocardial infarction with single-vessel disease accompanied by precordial ST-segment depression; and group II (n = 10), inferior myocardial infarction with multi-vessel disease. The subjects underwent 12-lead exercise electrocardiography, stress Tl-201 myocardial imaging and stress radionuclide ventriculography. Exercise-induced precordial ST-segment depression observed in group Ib was associated with large infarction and infarction extending into the inferoseptal wall of the left ventricle on myocardial image. On stress ventriculography, worsening of the septal wall motion was more frequently observed in group Ib than in group Ia. Coronary arteriography revealed a higher rate of rich collateral vessels to the infarcted zone in group Ib than in group Ia. When we compared the diagnostic ability for detecting multi-vessel disease in prior inferior myocardial infarction, although sensitivity was not different among three tests, both exercise electrocardiography and radionuclide ventriculography had poor specificity and predictive value compared to stress Tl-201 myocardial imaging. Thus we concluded that exercise-induced precordial ST-segment depression observed in prior inferior myocardial infarction with single-vessel disease should reflect a peri-infarctional ischemia located in the inferoseptal wall of the left ventricle, and that stress Tl-201 myocardial imaging is the most accurate method for diagnosing multi-vessel disease in prior inferior myocardial infarction.

Effects of heart failure status on electrocardiogram precordial leads and their value for monitoring body fluid changes in heart failure patients

Changes in QRS morphology in ECG precordial leads and the value of these leads for identifying worsening heart failure (HF) have not been fully determined, though the effects of HF status on changes in QRS amplitude [1,2] and transitional zone [3,4] in these leads have been briefly described. When considering the right ventricle being more compliant than the left, it would be expected that expansion of the right ventricle is more than the left under the volume overload in worsening HF, and vice versa at its recovery [5], causing changes in QRS morphology in precordial leads. This study examined the effects of changes in HF status on the S-wave in the right precordial leads [6], R-wave in the left precordial leads [7], and the transitional zone of precordial leads [3,4], and compared these ECG variables with b-type natriuretic peptide (BNP) [8]. For the purposes of this study, we used a data base of monitoring HF patients between June 2003 and March 2009 [2,9]. The ECG data were included based on the availability of complete data set of both triplets of ECGs and simultaneous clinical data at the time of clinical stability, worsening, and recovery of HF. ECGs of bundle branch blocks were excluded. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [10]. At every visit to the clinic, patients were examined for HF-related symptoms/signs [11]. Additional regular evaluation includedwhether or not the presence of significant fluid weight gain [9], ultrasonographic pleural effusion [12,13], and 3-fold increase in BNP compared to clinical stability [14]. Worsening HF event was diagnosed if two or more combinations of signs/tests appeared. Asymptomatic HF event was defined as the absence of changes in symptoms other than ankle edema between two consecutive clinic visits, despite the appearance of body fluid retention disclosed by a clinician [2,15]. Moderate to severe leg edema without any other symptomatic change was considered to be symptomatic event. The lead positions of precordial ECGwere described elsewhere [16]. Voltage amplitudes were evaluated for the S-wave in V1/V2, sum of these 2 leads, R-wave in V5/V6, and sum of these 2 leads by averaging 5 consecutive beats. The position of the transitional zone was determined by the change from predominantly negative QRS to predominantly positive one. The transitional zone situated at the place between two adjacent leads was made by interpolation, e.g., V3.5[16]. Continuous variables are presented as means (SD), and were compared with ANOVA with post hoc Bonferronis correction for multiple comparisons among baseline, worsening of HF, and recovery fromHF. Discriminate properties of changes in ECG variable(s) and BNP from clinical stability to worsening HF were evaluated using receiver operating characteristic (ROC) curve analysis. For ROC analysis, three data sets obtained at the time of clinical stability, worsening, and recovery of HF were used. For each ROC curve, a cut-off point was determined for ECG variable(s) and %Δ of BNP that maximized the sum of the sensitivity and specificity for discriminating changes obtained fromclinical stability toworseningHFand changes under decongestion/ stable HF status [2]. In view of multiple t tests for comparison between data from pairs from the 3 HF status states, a significant difference was taken as pb0.016 (Bonferronis correction). From a total of 83 ambulatory patients with established HF who were enrolled and followed up, 31 had available ECGs and HF-related clinical data for the analysis. The demographic features of the 31 study patients with clinical stability at study entry are summarized in Table 1. Features noted to confirm the diagnosing of worsening of HF status in the 31 patients are presented in Table 2. As shown, there were 35 worsening HF events, of which 19 were symptomatic, and 16 asymptomatic. As shown in Table 3, there was no significant difference in the mean S-wave depth in V1/V2, and the height of R-wave in V5/V6, and each sum of 2 leads among clinical stability, worsening HF, and its recovery. The transitional zone shifted to the left from clinical stability to worsening HF, and returned to the position nearly corresponding to the