Incidence, mechanisms, treatment, and outcomes of donor vessel injury during percutaneous coronary interventions for chronic total occlusion.

BACKGROUND: Donor vessel injury is a potentially life-threatening complication of chronic total occlusion (CTO) percutaneous coronary intervention (PCI). AIMS: Our goal was to examine the incidence, mechanisms, treatment, and outcomes of patients with donor vessel injury in a large multicenter CTO PCI registry. METHODS: We analyzed the baseline clinical and angiographic characteristics, and procedural outcomes of 12,349 CTO PCIs performed between 2012 and 2022 at 44 centers. RESULTS: The incidence of donor vessel injury was 0.35% (n = 43). The baseline clinical characteristics of patients with and without donor vessel injury were similar. Cases complicated by donor vessel injury were more complex with higher Japanese CTO score (2.9 ± 1.1 vs. 2.4 ± 1.3; p = 0.004) and lower procedural success rate (69.8% vs. 85.2%; p = 0.004). The retrograde approach was used more commonly in donor vessel injury cases (68.9% vs. 30.9%; p < 0.001). Most (53.5%) donor vessel injuries were guide catheter-induced, whereas 20.9% were due to donor vessel thrombosis. Of the 43 patients with donor vessel injury, 36 (83.7%) were treated with stenting and seven (16.3%) received a left ventricular assist device. The incidence of major adverse cardiovascular events (MACEs) was significantly higher in cases with donor vessel injury (23.3% vs. 2.0%; p < 0.001). Of the 43 patients with donor vessel injury, five patients (11.6%) experienced acute myocardial infarction and four patients (9.3%) died. CONCLUSIONS: Donor vessel injury, occurred in 0.35% of CTO PCIs performed by experienced operators, was mainly due to guide catheter-induced dissection or thrombosis and was associated with lower procedural success and higher MACE.

Comparative effects of high-dose atorvastatin versus rosuvastatin on lipid parameters, oxidized low-density lipoprotein, and proprotein convertase subtilisin kexin 9 in acute coronary syndrome.

AIM: Current guidelines recommend administration of high-dose statins in acute coronary syndrome (ACS). It has been reported that statins upregulate proprotein convertase subtilisin kexin 9 (PCSK9) mRNA expression and increase circulating PCSK9 levels. We aimed to compare the effects of high-dose atorvastatin and rosuvastatin on serum oxidized low-density lipoprotein (oxidized-LDL) and PCSK9 levels in statin-naive patients with ACS. PATIENTS AND METHODS: One hundred and six patients with ACS were enrolled in this study. The patients were assigned randomly to receive atorvastatin (80 mg/day) or rosuvastatin (40 mg/day) by using a ratio of 1 : 1 in randomization. The levels of total cholesterol (TC), triglyceride, high-density lipoprotein cholesterol, LDL-cholesterol, oxidized-LDL, and PCSK9 were compared between groups after a 4-week treatment. RESULTS: Our study population included 53 patients in the atorvastatin group (age: 58.13±11.30 years, 11.32% female) and 53 patients in the rosuvastatin group (age: 59.08±12.44 years, 15.09% female). In both groups, lipid parameters, oxidized-LDL, and PCSK9 values changed significantly according to the baseline following treatment. High-dose atorvastatin and rosuvastatin induced similar decreases in LDL-cholesterol, oxidized-LDL, and triglyceride levels and similarly increased in high-density lipoprotein cholesterol and PCSK9 levels (P>0.05). CONCLUSION: We showed that atorvastatin and rosuvastatin treatment regimens have comparable effects on lipid parameters and PCSK9 levels in ACS patients.

A nation-wide survey of patients with homozygous familial hypercholesterolemia phenotype undergoing LDL-apheresis in Turkey (A-HIT 1 registry).

BACKGROUND AND AIMS: Homozygous familial hypercholesterolemia (HoFH) is a genetic condition characterized by lethally high levels of low-density lipoprotein cholesterol (LDL-C) from birth, and requires rapid and aggressive intervention to prevent death due to coronary heart disease and/or atherosclerosis. Where available, lipoprotein apheresis (LA) is the mainstay of treatment to promote survival. METHODS: A-HIT1 registry was conducted with the aim of providing insight to the real-life management of HoFH patients undergoing LA in Turkey, where LA procedures are fully reimbursed and widely available. Participating centers provided patient information, including family history, treatment patterns and relevant laboratory values, via a standard questionnaire. RESULTS: The study evaluated 88 patients (mean age: 27 ±â€¯11 years, 41 women) in 19 centers. All patients were receiving regular LA with a clinical diagnosis of HoFH. Mean age at first symptom disease was 10 ±â€¯10 years, and at diagnosis it was 12 ±â€¯11 years; 74.7% were diagnosed before age 15 years; and only 31% before the age of 7. First referral of most patients was to pediatricians. Early onset coronary artery disease was present in 57.8% of patients. Mean age at first LA was 21 ±â€¯12 years. Only 11 (12.5%) patients were undergoing LA weekly. Mean frequency of apheresis sessions was 19 ±â€¯13 days. For the last four LA sessions, LDL-C levels reached the target in only in 5.7% of patients. CONCLUSIONS: Diagnosis of HoFH is delayed, and LDL targets are not reached. LA frequencies are not optimal. Urgent attention is needed to support the survival of patients with HoFH.

New parameters in identification of right ventricular myocardial infarction and proximal right coronary artery lesion.

OBJECTIVE: The diagnosis of right ventricular myocardial infarction (RVMI) accompanied by acute inferior myocardial infarction (MI) is still a problem that we encounter. This study was designed to find out the usefulness both of peak myocardial systolic velocity (Sm) and of the myocardial performance index (MPI) of the right ventricle measured by pulsed-wave tissue Doppler imaging (TDI) in assessing right ventricular function. METHODS: Sixty patients who experienced a first acute inferior MI (mean [+/- SD] age, 57 +/- 9 years) were prospectively assessed. An ST-segment elevation of >or= 0.1 mV in V(4)-V(6)R lead derivations was defined as an RVMI. From the echocardiographic apical four-chamber view, the Sm, the peak early diastolic velocity, peak late diastolic velocity, the ejection time, the isovolumetric relaxation time, and the contraction time of the right ventricle were recorded at the level of the tricuspid annulus by using TDI. Then, the MPI was calculated. The patients were classified into the following three groups, according to the localization of the infarct-related artery (IRA) detected using coronary angiography: group I, proximal right coronary artery; group II, distal right coronary artery; and group III, circumflex coronary artery. RESULTS: RVMIs were detected in sixteen patients, and the IRA in 27 patients was the proximal right coronary artery. The right ventricular Sm was observed to be significantly low in patients with RVMIs and those in group I compared to those without RVMIs and those in groups II and III (10.9 +/- 1.3 vs 14.3 +/- 3.2 cm/s, respectively [p < 0.001]; 11.5 +/- 2.5 vs 15.1 +/- 3 cm/s, respectively; and 14.9 +/- 2.6 cm/s, respectively [p < 0.001]). In the diagnosis of RVMI, the values for sensitivity, specificity, negative predictive value, and positive predictive value of Sm < 12 cm/s were 81%, 82%, 92%, and 62% respectively, and in the diagnosis of the proximal right coronary artery as the IRA, those values were 63%, 88%, 74%, and 81%, respectively. The MPI was high in the same patient groups (0.83 +/- 0.12 vs 0.57 +/- 0.11 in those patients without RVMI, respectively, [p < 0.001]; 0.74 +/- 0.13 vs 0.56 +/- 0.15 in group II and 0.54 +/- 0.07 in group III, respectively [p < 0.001]). The sensitivity, specificity, negative predictive value, and positive predictive value of an MPI of > 0.70 in the diagnosis of RVMI were calculated as 94%, 80%, 97%, and 63%, respectively, and in the diagnosis of the proximal right coronary artery as the IRA, those values were 78%, 91%, 83%, and 88% respectively. CONCLUSIONS: An Sm <12 cm/s and an MPI > 0.70 obtained by TDI may define RVMI concomitant with acute inferior MI, and the IRA.

Analysis of the myocardial velocities in patients with mitral stenosis.

BACKGROUND: Pure mitral stenosis (MS) affects left-ventricular performance as a result of myocardial and functional factors. We planned this study to evaluate the effect of MS on right- and left-ventricular functions using Doppler tissue imaging (DTI). METHODS: A total of 46 patients with an established diagnosis of MS (mean age: 41 +/- 11 years), and 40 age-matched healthy individuals (mean age: 40 +/- 9 years) were included in this study. Echocardiography equipped with DTI function was performed on each participant. The mitral valve area was measured. Myocardial velocities were recorded at 4 different sites (septum, lateral, anterior, and inferior) of the left ventricle, and the right-ventricular free wall annulus by DTI. The positive systolic velocity when the mitral and tricuspid ring moved toward the cardiac apex, and 2 negative diastolic velocities when the mitral annulus moved toward the base away from the apex (1 during the early phase of diastole and another in the late phase of diastole [A(m)]) were measured. The early diastolic velocity/A(m) ratio was calculated for each wall. The mean of systolic and diastolic myocardial velocities of the left ventricle was calculated. Patients with pure MS were compared with healthy participants, and the relationship of DTI variables with mitral valve area was evaluated. RESULTS: The myocardial velocities of the left ventricle indicating left-ventricular function were found to be significantly lower in patients with pure MS. Right-ventricular annulus velocities, on the other hand, were similar in both groups. A significant positive correlation could be established between mitral valve area and mean positive systolic velocity, A(m) of the left ventricle, and right-ventricular A(m) (r = 0.50, P <.001; r = 0.48, P =.001; r = 0.45, P =.002, respectively), whereas a significant negative correlation (r = -0.42, P =.004) was established for right-ventricular early diastolic velocity/A(m) ratio. CONCLUSION: This first study where pure MS was evaluated by DTI shows that MS affects left-ventricular performance on long axis. The results indicate that the decrease in left-ventricular performance is caused by both functional and myocardial factors.

Thrombolysis in myocardial infarction frame count with angiographically normal coronary arteries and its relationship to ST-segment depression.

BACKGROUND: The thrombolysis in myocardial infarction frame count (TFC) has been proposed as a simple, reproducible, objective and quantitative method to assess coronary blood flow. However, the TFC in normal coronary arteries has not been investigated in detail. The aim of this study was to determine normal TFC values and investigate their correlation with ST-segment depression during exercise testing (ET). METHODS AND RESULTS: The TFC was measured in 116 cases with normal coronary arteries who underwent ET. The ST segment was evaluated on 12-lead electrocardiograms at 60 ms after the J-point. Horizontal or downsloping ST-segment depression of > or = 0.5 mm was recorded and the sum of the depressions was calculated. When ST-segment depression > or = 1 mm compared to the level of PR segment on two or more leads was detected, the test was accepted as positive. The TFC for the left anterior descending coronary artery (LAD) was significantly higher than those for the left circumflex coronary artery (LCx) and the right coronary artery (RCA). The TFC of coronary arteries was significantly higher in patients with ET positive (for LAD, 39.5 +/- 10.7 compared with 30.1 +/- 7.6 frames; for LCx, 29.2 +/- 9.3 compared with 23.6 +/- 6.5 frames; and for RCA, 30.7 +/- 11 compared with 23.7 +/- 7 frames; P < 0.001 for overall comparisons). Women had a lower TFC than men in the LAD. Moreover, it was determined that the TFC values for the LAD, LCx and RCA significantly correlated with the sum of ST-segment depression (r = 0.57, r = 0.46 and r = 0.41, respectively, P < 0.001 for overall correlations). It was also determined that the TFC was affected by the proximal diameter of the coronary arteries. CONCLUSIONS: The results of this study highlight the differences of the TFC in normal LAD, LCx and RCA. In patients with normal coronary arteries, the fact that the TFC is higher in ET-positive than in ET-negative patients may explain false positive results of ET. Sex and coronary artery diameter should be taken into consideration in evaluating the TFC.

Effect of postmenopausal hormone replacement therapy on cardiovascular performance.

UNLABELLED: Postmenopausal hormone replacement therapy (HRT) has usually been evaluated the relationship with atherosclerotic disease, whereas its effect on direct cardiac functions hasn't been investigated in detail. This study was planned to investigate the long-term effects of HRT on cardiac functions and exercise performance. METHODS: Thirty-six postmenopausal women (mean age: 51 +/- 4 years, 39-60 years) were prospectively analyzed with pulsed wave Doppler echocardiography and symptom-limited exercise stress test before HRT (oral 0.625 mg conjugated estrogen and 2.5 mg medroxyprogesteron acetate/day), and at the third and the sixth months. The effect of HRT on left ventricular ejection fraction (EF), early filling velocity (E wave) and late filling velocity (A wave), E wave deceleration time (EDT), E/A ratio, myocardial performance index (MPI), exercise duration and METS changes were examined. RESULTS: HRT did not significantly alter the left ventricular EF. At the third month of HRT, there was an insignificant increase in E wave, EDT, and E/A ratio, whereas an insignificant decrease was noted in MPI (P > 0.05). However, at the sixth month of HRT, these changes became significant (68 +/- 12 vs. 75 +/- 13 cm/s, P < 0.01; 171 +/- 24 vs. 184 +/- 14 ms, P < 0.01; 1.01 +/- 0.23 vs. 1.11 +/- 0.27, P < 0.01, and 44 +/- 9 vs. 39 +/- 8%, P < 0.001, respectively). On the other hand, exercise duration and exercise METS values showed significant improvements at the third month of HRT (423 +/- 104 vs. 482 +/- 104 s, P < 0.001; 8.2 +/- 1.7 vs. 9.1 +/- 2 METS, P < 0.001). These improvements also continued at the sixth month of HRT. In conclusion, postmenopausal HRT leads to a progressive improvement on left ventricular function parameters, and in parallel, in exercise performance.

New parameters in the interpretation of exercise testing in women: QTc dispersion and QT dispersion ratio difference.

BACKGROUND: It has been reported that the increase of QT dispersion (QTD) that occurs due to increased inhomogeneity of the ventricular repolarization because of transient ischemia obtained by standard 12-lead electrocardiogram (ECG), the changes during exercise, and the differences between exercise and rest increase the accuracy of exercise test in the diagnosis of coronary artery disease (CAD). HYPOTHESIS: This study was designed to investigate the value of QTD parameters, which are reported to increase the diagnostic accuracy of exercise test in women. METHODS: Ninety-seven women who had undergone coronary angiography and exercise test were evaluated for diagnosis of chest pain. QT dispersion was calculated using the measurements of the highest and lowest values of QT interval obtained by ECG during peak exercise. The QTc using Bazett's equation, and the QTD ratio (QTDR) using QT/RR were calculated, and QTcD and QTD ratios were obtained. The difference between QTcD and QTDR was determined by extracting the rest values from the exercise values. RESULTS: The groups with normal coronaries (n = 48), single-vessel CAD (n = 24), and multivessel CAD (n = 25) were compared. The obtained QTD parameters at peak exercise and their differences between exercise and rest were found to be significantly increased in patients with CAD (p <0.001). Furthermore, these parameters were found to be higher in the patients with multivessel CAD than in those with single-vessel disease (p < 0.05). With the parameters QTcD > 60 ms and QTDR > 10%, greater sensitivity and specificity were obtained compared with ST-segment depression. The highest diagnostic accuracy was obtained with the QTD parameters calculated from the differences between rest and exercise values. The diagnostic accuracy of the difference of QTcD > 15 ms and the difference of QTDR > 5% was relatively higher than the other parameters (sensitivity, specificity, and negative and positive predictor values are 84, 88, 84, 87% and 84, 96, 85, 95%, respectively). CONCLUSION: The use of QTD parameters as variables of ECG, which is easily obtainable in the evaluation of exercise ECG in women, increases the diagnostic accuracy of the exercise test. In addition, the evaluation of QTD variables may provide information about the incidence of CAD.

The effect of Valsalva maneuver on P wave in 12-lead surface electrocardiography in patients with paroxysmal atrial fibrillation.

The previous studies relating to the effect of the Valsalva maneuver on P wave do not provide detailed information. In those studies, the parameters related to P wave duration during the release phase of the Valsalva maneuver were evaluated. The authors evaluated P wave amplitude as well as P wave duration during the strain phase of the Valsalva maneuver. Thirty-seven normal subjects and 36 patients with paroxysmal atrial fibrillation (PAF) were included in the study. Twelve-lead surface electrocardiography (ECG) was obtained from all the patients before and during the strain phase of the Valsalva maneuver. The authors evaluated the parameters related to both P wave duration and P wave amplitude. The highest P wave voltage was expressed as the P wave amplitude maximum (P amp max), the lowest P wave voltage as the P wave amplitude minimum (P amp min), and the P wave amplitude dispersion (P amp dispersion) as "the P amp max - the P amp min." Also, the maximum P wave duration was expressed as the P maximum (P max), the minimum P wave duration as the P minimum (P min), and the P wave dispersion as "the maximum P wave duration (P max) - the minimum P wave duration (P min)." All these parameters were measured before and during the strain phase of the Valsalva maneuver. P max, P dispersion, P amp max, and P amp dispersion were higher in patients with PAF compared to those of normal subjects before the Valsalva maneuver. In normal subjects, P max, P wave dispersion, P amp max, and P amp dispersion values were significantly higher in the strain phase of the Valsalva maneuver than before (p<0.01, p<0.01, p<0.05, and p<0.05, respectively). In the patients with PAF, P max, P wave dispersion, P amp max, and P amp dispersion values were significantly lower during the strain phase of the Valsalva maneuver than before. In conclusion, in the patients with PAF, P wave parameters were decreased during the strain phase of the Valsalva maneuver, approaching to the normal levels.

Can P wave parameters obtained from 12-lead surface electrocardiogram be a predictor for atrial fibrillation in patients who have structural heart disease?

This study was planned to investigate the parameters detecting risk of developing atrial fibrillation (AF) in patients with sinus rhythm with structural heart disease. Forty-five patients with AF and 37 patients without AF but with structural heart disease (Group I) were included in this study. Thirty-eight patients (Group II) had successfully undergone medically or electrically cardioversion after transesophageal echocardiography. The restoration of sinus rhythm could not be achieved in 7 patients who were excluded from this study. After providing sinus rhythm, amiodarone was given orally to the patients to prevent recurrences. Left ventricular ejection fraction (LVEF) was calculated and left atrial diameter (LAD) was measured by echocardiography in group I and in group II after cardioversion. A 12-lead electrocardiography (ECG) was simultaneously obtained from all the patients. In these ECG recordings, maximum P wave duration (P max), minimum P wave duration (P min), and P wave dispersion (P dispersion) were calculated. P dispersion was expressed as "P max-P min." Also, the highest P wave voltage is expressed as P amplitude maximum (P amp max), the lowest P wave as P amplitude minimum (P amp min), and P amplitude dispersion (P amp dispersion) was calculated as the difference of both. In univariate analysis, P max, P dispersion, P amp max, P amp dispersion, LAD, LVEF, and old age were significant predictors of chronic AF (p < 0.001, p < 0.01, p < 0.01, p < 0.01, p = 0.003, p = 0.02, and p = 0.01, respectively). However, in multivariate analysis, P max and LAD were independent predictors of chronic AF in patients with structural heart disease (r = 0.39, p < 0.05; r = 0.34; p < 0.05, respectively). In conclusion, in estimating the risk of developing chronic AF, P max and LAD are predictive parameters in patients with sinus rhythm with structural heart disease.

[Evaluation of "admission index of insulin resistance (AIRI)" as an early stage risk predictor in nondiabetic acute coronary syndromes]. / Diyabetik olmayan akut koroner sendromlarda erken dönem yeni bir risk onbelirleyicisi olarak "gelis insülin rezistans indeksi (GIRI)'nin" degerlendirilmesi.

OBJECTIVE: Insulin resistance is a risk predictor for many cardiovascular diseases, but its effect on etiology and prognosis of diseases has not been clearly identified. In this study, we aimed to investigate whether admission index of insulin resistance (AIRI), recently and practically presented for determination of insulin resistance, could be a new risk predictor of early prognosis in nondiabetic acute coronary syndromes. METHODS: One hundred and sixty nondiabetic patients admitted to the intensive coronary care unit and underwent coronary angiography with the diagnosis of acute myocardial infarction (AMI) (Group I; 72 patients; mean age - 58+/-12 years) or unstable angina pectoris (UAP) (Group II; 88 patients; mean age 58+/-10 years) were included in the study. In all patients blood glucose and insulin levels were measured on admission and AIRI was calculated by the formula of "admission glucose level X insulin level / normal blood glucose level (5 mmol/L) X normal insulin level (5 mU/L)" for each patient. After determining the left ventricular ejection fraction (LVEF) and wall motion score index (LVWMSI) echocardiographically and calculating the Gensini score index from coronary angiography, the patients were followed up for major cardiac events (heart failure, atrial fibrillation, reinfarction, life-threatening ventricular arrhythmias, atrio-ventricular block, need for revascularisation and mortality) for 30 days. RESULTS: AIRI was found higher in Group I (7.2+/-5.3 versus 5.2+/-4.4, p< 0.01) than in Group II. AIRI was positively correlated with Gensini score and LVWMSI (r=0.41, p<0.01 and r=0.48, p<0.001, respectively) and negatively correlated with LVEF (r=-0.37, p=0.001) in Group I. In addition, it was seen that positive correlation of AIRI with Gensini score (r=0.23, p=0.01) and LVWMSI (r=0.43, p=0.0001) in Group I persisted on multivariate regression analysis. Again, AIRI was significantly correlated with heart failure (r=0.42, p<0.0001), atrial fibrillation (r=0.35, p=0.002) and reinfarction (r=0.23, p=0.04) in Group I. Along with this, in multivariate regression analysis, it was correlated with heart failure (r=0.21, p<0.007), atrial fibrillation (r=0.18, p=0.01) and reinfarction (r=0.18, p=0.01). On the other hand, there was no significant correlation between AIRI and these parameters in Group II. CONCLUSION: AIRI can be used in early stage as a risk predictor to determine high-risk subgroups of nondiabetic patients presenting with AMI. Also AIRI, a parameter, which is practically calculated and easily used, is an independent risk factor detecting the extent of coronary artery disease and left ventricular dysfunction in patients with AMI.

[Left ventricular hypertrophy increases the frequency of ventricular arrhythmia in hypertensive patients]. / Sol Ventrikül Hipertrofisi Hipertansif Hastalarda Ventriküler Aritmi Sikligini Arttiriyor.

OBJECTIVE: To evaluate the relationship between left ventricular hypertrophy (LVH) and geometrical structure of the left ventricle with the risk of arrhythmia and QT dispersion (QTd) in hypertensive patients. METHODS: Eighty patients were included (mean age 53 +/- 11 years, 45 women) in the study. Among them, concentric LVH was present in 30, concentric remodelling in 15 and normal left ventricular geometry in 35 patients. Twenty-four hours electrocardiographic monitoring and QTd calculation were performed for all patients. RESULTS: Lown grade 2-3 ventricular arrhythmia was found in 30 patients (37%) and Lown grade 4a-4b ventricular arrhythmia was documented in 17 patients (21%). The frequency of >Lown 2 ventricular arrhythmia in patients with concentric LVH was significantly higher than those of the subjects with concentric remodelling or normal geometry (p<0.01). The percentage of >Lown 2 ventricular arrhythmias were 80% in patients with LVH and 10% in patients without LVH. QT and QTc dispersions in patients with concentric hypertrophy were significantly longer than those of the patients with concentric remodelling and normal geometry. Additionally, QT and QTc dispersions in patients with ventricular arrhythmias were more frequent than in those without (p<0.001). The left ventricular mass index correlated positively both with the QTd and the QTc dispersions (r=0.33, p=0.007, r=0.26, p= 0.03, respectively). The left ventricular mass index also correlated significantly with both grades (Lown 2-3 and Lown 4a-4b) of ventricular arrhythmia (r=0.59, p=0.001; r=0.53, p=0.001, respectively). CONCLUSION: In hypertensive patients, especially in those with concentric LVH, the incidence of ventricular arrhythmia increases in relation with QT dispersion.

The effect of diabetes mellitus on the P-wave dispersion.

BACKGROUND: P-wave dispersion (PD), a measure of heterogeneity of atrial refractoriness, is defined as the difference between the minimum (P min) and maximum P-wave (P max) durations on standard 12-lead electrocardiography (ECG). Increase in PD shows the intra-atrial and inter-atrial non-uniform conduction. In the present study the evaluation of the effect of diabetes mellitus (DM) on PD in patients without coronary artery disease and hypertension was carried out. METHODS AND RESULTS: Seventy-six diabetic patients who had no coronary artery disease or hypertension (group 1; mean age 48+/-9) and 40 healthy volunteer individuals (group 2; mean age 46+/-13) were enrolled in the study. After obtaining 12-lead surface ECG of all cases, P max and P min P-wave durations were measured and the differences between them were taken as PD (PD=P max-P min). Left atrium diameter, left ventricular end systolic and end diastolic diameters were measured and left ventricular ejection fraction was determined by echocardiography. Pulse wave mitral flow velocities were measured from the apical 4-chamber view. Mitral early diastolic velocity (E), late diastolic velocity (A), E/A, E deceleration time and isovolumetric relaxation time were determined. In comparison of the 2 groups there was no statistically significant difference among age, sex, systolic and diastolic blood pressure, resting heart rate and body mass index of the cases. Although PD and P max were significantly higher in diabetic patients, there was no difference between P min values (33+/-12 vs 28+/-10, p=0.02; 99+/-12 vs 93+/-10, p=0.011; 66+/-9 vs 65+/-10, p=NS; respectively). CONCLUSIONS: DM might increase PD even without ischemia, hypertension and left ventricular hypertrophy.

Comparison of pulmonary venous flow velocities and left ventricular diastolic and ejection time in patients with moderate mitral and aortic stenosis. Pulmonary venous flow velocities in mitral and aortic stenosis.

BACKGROUND: Doppler pulmonary venous flow velocities (PVFV) pattern are useful parameters in assessing the left ventricular diastolic functions. Both mitral stenosis (MS) and aortic stenosis (AS) lead to diastolic dysfunction. We compared PVFV and left ventricular diastolic and ejection time (ET) in patients with moderate MS and AS. METHODS: Forty-three patients with moderate MS (group 1), 65 patients with moderate AS (group 2), and 33 healthy subjects as controls (group 3) were included in this study. After obtaining standard measurements echocardiographically, diastolic period (DP), ET, the ratio of the DP to the ET (DP/ET), isovolumetric contraction time (ICT), isovolumetric relaxation time (IRT), peak systolic flow velocity (PS), peak antegrade diastolic flow velocity (PD), peak reversal flow velocity at atrial contraction (PRA), the ratio of the peak systolic to the diastolic flow velocity (PS/PD), deceleration time of the antegrade diastolic flow (PDDT), and pressure half time of the peak antegrade diastolic flow velocity (PDPHT) were measured. Mitral valve area (MVA), aortic valve area (AVA), systolic pulmonary artery pressure (PAP), peak and mean gradients were calculated with standard formulas. RESULTS: In univariate analysis, MVA was correlated with PDPHT and PDDT (r = -0.41; p < 0.01, r = -0.36; p < 0.05, respectively), also it was correlated with DP/ET (r = -0.57; p < 0.001). Mitral peak and mean diastolic gradient were correlated with PS/PD (r = -0.43; p < 0.01, r = -0.36; p < 0.05, respectively) and DP/ET (r = 0.51; p < 0.01, r = 0.46; p < 0.01, respectively). AVA was only correlated with DP/ET (r = 0.38; p < 0.05). Aortic peak and mean systolic gradient were correlated with PS/PD (r = -0.29; p < 0.05, r = -0.27; p < 0.05, respectively) and DP/ET (r = -0.38; p < 0.01, r = -0.40; p < 0.01, respectively). In the same analysis, PAP in patients in group 1 and 2 was correlated with PS/PD (r = -0.42; p < 0.01 and r = -0.40; p < 0.01, respectively) and also it was correlated with PD (r = 0.37; p < 0.05 and r = 0.27; p < 0.05, respectively) in both groups. CONCLUSION: Moderate MS and AS similarly affect the PVFV, and PS/PD correlates with hemodynamics similarly both in MS and AS. Nevertheless, PDDT and PDPHT correlate with solely MVA. IRT higher in AS than MS, though DP/ET and ICT higher in MS than AS, and DP/ET relates with the severity of both MS and AS.

Does the myocardial performance index affect pulmonary artery pressure in patients with mitral stenosis? A tissue Doppler imaging study.

BACKGROUND: The relation between systolic pulmonary artery pressure (PAP) and mitral stenosis (MS) has been poorly understood. Although the mitral valve area (MVA) is an important factor affecting the PAP, there is a wide spectrum of the PAP in patients with MS despite a similar MVA. So, we analyzed whether the left and right ventricular myocardial performance index (MPI) correlated with the PAP. METHODS: Two-dimensional Doppler echocardiography was performed in 46 patients with MS. The left atrial diameter, mean mitral gradient, and MVA were measured. The PAP was derived from the tricuspid regurgitant jet velocity. The ejection time (ET), isovolumetric relaxation time (IRT), and contraction time (ICT) were measured on annulus of interventricular septum, lateral, inferior and anterior wall of left ventricle, and right ventricle free wall from apical two- and four-chamber views in patients with MS and 40 age-matched healthy patients by tissue Doppler imaging (TDI). Then the MPI was calculated as (IRT + ICT)/ET for both left and right ventricle. The correlation of PAP with MVA, mean mitral gradient, left atrial diameter, and left and right ventricular MPI was evaluated. RESULTS: MVA and PAP were measured as 1.57 +/- 0.39 cm2 (0.8-2.5 cm2)and 42 +/- 16 mmHg, respectively. It was determined that the MPI increased in patients with MS(0.59 +/- 0.1 vs 0.48 +/- 0.07, P < 0.001). It was also demonstrated that the MVA, left atrial diameter, mean diastolic gradient, and left ventricular MPI were correlated with PAP(r =-0.39 [P = 0.007], r = 0.43 [P = 0.003], r = 0.58 [P < 0.001], and r = 0.65 [P < 0.001], respectively). In multivariate analysis, although the PAP correlated with mean diastolic gradient and MPI (r = 0.39 [P = 0.013], and r = 0.48 [P < 0.001]), it did not correlate with left atrial diameter and MVA. The PAP also correlated with right ventricular MPI(r = 0.63 [P < 0.001]). CONCLUSION: This study demonstrates that the left ventricular MPI obtained by TDI is an important marker of PAP, and right ventricular MPI correlates with the PAP in patients with MS.

A subacute left ventricular free wall rupture after thrombolytic and glycoprotein IIb/IIIa inhibitor treatment: an overlooked finding of left ventriculography.

Subacute left ventricular free wall rupture is a rare complication in acute myocardial infarction. With the increasing use of thrombolytic agents and glycoprotein IIb/IIIa inhibitors, this complication has been increasing recently. We report a case of subacute cardiac rupture with frank pericardial effusion receiving thrombolytic and glycoprotein IIb/IIIa inhibitor therapies.

A case of catecholamine induced heart failure with left ventricular hypertrophy accompanied by mid-ventricular obstruction.

A 36 year old Turkish female patient complaining of widespread redness of the skin, shortness of breath, palpitations, nausea, hum and reverberation in the head was examined. The patient was diagnosed with catecholamine induced hypertension, which was caused by paraganglionoma. In addition, left ventricular concentric hypertrophy accompanied by systolic gradient in mid-ventricle, which is rarely observed, was determined by echocardiography. Hypertensive attacks and mid-ventricular systolic gradient disappeared after surgery. This case shows that one of the causes of the heart failure due to catecholamine releasing tumors can be left ventricular obstruction.

Effects of long-term hormone replacement therapy on QT and corrected QT dispersion during resting and peak exercise electrocardiography in post-menopausal women.

It is known that the QT interval is longer in women than men. Estrogen is reported to account for the QT interval prolongation in several studies conducted with hormone replacement therapy (HRT) in postmenopausal women. Along with this, there are conflicting data as regards the effects of HRT on QT interval and dispersion. Moreover, there is no evidence about the effect of HRT on exercise QT parameters. We compared QT parameters obtained from surface electrocardiograms during resting and peak exercise before and after 6 months of HRT consisting of estrogen plus progesterone in healthy postmenopausal women. Twenty-four healthy postmenopausal women were given 0.625 mg/day conjugated estrogens and 2.5 mg/day medroxyprogesterone acetate for 6 months. Exercise stress testing using the Bruce protocol was performed before and after HRT. QT maximum, minimum, dispersion and corrected QT maximum, minimum and dispersion were calculated during resting and peak exercise. HRT resulted in a significant increase in estradiol plasma levels from 24+/-10 pg/mL to 117+/-66 pg/mL (P<0.001). There was no significant difference in resting QT parameters after HRT, whereas QT dispersion and corrected QT dispersion were significantly increased during peak exercise (20+/-7 versus 25+/-10 ms; P<0.05, 33+/-12 versus 41+/-16 ms; P<0.05, respectively). Nonetheless, the other exercise QT parameters were unchanged. The resting QT parameters are not affected by long term HRT consisting of estrogen plus progesterone, which leads to an increase in QT dispersion and corrected QT dispersion during peak exercise.

Value of the corrected QT interval dispersion obtained exercise electrocardiography in determining remote vessel disease in patients with healed Q-wave myocardial infarction.

BACKGROUND: QT and corrected QT dispersion (QTD, QTcD) obtained by using the standard 12-lead ECG is a marker of nonhomogenous ventricular repolarization. QTD obtained from exercise ECG increases the diagnostic reliability of ST-segment changes. The aim of this study was to investigate the diagnostic accuracy of the QTD and QTcD obtained by a 12-lead ECG during the peak exercise in determining remote vessel disease in patients with healed Q-wave MI. METHODS: Eighty patients with healed Q-wave MI (mean age 54 +/- 8 years; 71 men, 9 women; 29 anterior; 51 inferior MI) who underwent exercise stress testing and coronary angiography were included in this study. Patients were divided into two groups, with (group I) and without (group II) remote vessel coronary artery disease. During peak exercise, sensitivity, specificity, negative and positive predictive value of the ST-segment depression, and QTcD were compared between both groups. Moreover, the resting and peak exercise ECG parameters were compared between group I and group II. RESULTS: In coronary angiography, remote vessel disease was detected in 48 patients (group I). In determining remote vessel disease, the sensitivity, specificity, and the negative and positive predictive values of the peak exercise QTcD > or = 70 ms were significantly higher than those of the peak exercise ST-segment depression (81%, 63%, 69%, and 76% vs 71%, 53%, 55%, and 69%, respectively; P < 0.01 for all comparisons). In group I, QTD and QTcD were significantly higher in patients with anterior wall MI than those with inferior wall MI both during the resting and peak exercise ECG. In group II, the resting QTD and QTcD were significantly higher in patients with anterior wall MI than those with inferior wall MI. In patients with anterior wall MI and inferior wall MI, QTD and QTcD significantly increased with exercise in group I. CONCLUSION: In patients with healed Q-wave MI, the value of QTcD > or = 70 ms increases the diagnostic accuracy of the exercise stress testing in determining remote vessel disease.

Is the beneficial effect of preinfarction angina related to an immune response?

Immune-mediated mechanisms are thought to play a key role in the development of coronary artery disease and its thrombotic complications. Preinfarction angina has been suggested to improve left ventricular function and short-term outcomes. The purpose of the present study was to investigate the relation between the immune response and in-hospital clinical course in preinfarction angina. We prospectively evaluated 93 patients. Forty-three patients exhibited preinfarction angina within 24 hours before the onset of acute myocardial infarction (AMI) (preinfarction angina group) and 50 patients were free from preinfarction angina (sudden onset group). The incidence of complications (heart failure, recurrent angina, arrhythmia and coronary interventions) and in-hospital mortality were assessed in the two study groups. We detected some immune markers, including white blood cells, C-reactive protein, immunoglobulins, and complement. White blood cells and CRP were significantly lower in the preinfarction angina group than in the sudden onset group (P < 0.001, P < 0.005, respectively). Conversely, IgE and C(4) were significantly higher in the preinfarction angina group than in the sudden onset group (P < 0.001, P < 0.001, respectively). The incidences of heart failure and severe arrhythmias were lower in the preinfarction group than in the sudden onset group (P < 0.005, P < 0.05 respectively). The beneficial effect of preinfarction angina may be associated with an immune-inflammatory response modified by a brief ischemic episode.