The outcome of peripartum cardiomyopathy patients-single center experience.

OBJECTIVE: Peripartum cardiomyopathy (PPCM) diagnosis made by excluding identifiable causes of heart failure (HF) and occurs end of the pregnancy or during the postpartum period of five months. It presents a clinical HF spectrum with left ventricular systolic dysfunction. BACKGROUND: The purpose of this study is to retrospectively evaluate the clinical characteristics, cardiac magnetic resonance (CMR) imaging features, and end-points consisting of left ventricle recovery, left ventricular assist device implantation, heart transplantation, and all-cause mortality. METHOD: Outpatient HF records between 2008 to 2021 were screened. Thirty-seven patients were defined as PPCM. Twenty-five patients had CMR evaluation at the time of diagnosis, and six patients were re-evaluated with CMR. RESULTS: The mean age was 30.5 ± 5.6 years, and the mean LVEF was 28.2% ± 6.7%. In 13(35.7%) patients, LVEF recovered during the follow-up course. The median recovery time was 281(IQR [78-358]) days. LVEF on CMR was 35.3 ± 10.5, and three patients exhibited late gadolinium enhancement(LGE) patterns. Sub-endocardial and mid-wall uptake pattern types were detected. 18(75%) patients met the Petersen left ventricle non-compaction cardiomyopathy(LVNC) criteria. Patients with NC/C ratio lower than 2.3 had lower LVEDVi and LVESVi (124.9 ± 35.4, 86.4 ± 7.5, p = .003; 86.8 ± 34.6, 52.6 ± 7.6, p = .006), respectively. The median follow-up time was 2129 (IQR [911-2634]) days. The primary endpoint-free 1-year survival was 88.9% (event rate 11.1%), and 5-year survival was 75.7% (event rate 24.3%). CONCLUSION: In a retrospective cohort of PPCM patients, 35.7% of patients' LVEF recovered, and the primary end-point of free-5-year survival was 75%. Twenty-five patients were assessed with CMR; three of four met the Petersen CMR-derived LVNC at initial evaluation.

Inferior ST-segment elevation due to metastatic cardiac tumor.

There are numerous causes for ST-segment elevation on ECG, the tumoral invasion of the heart being a rarer one. Because the management will differ one should always keep in mind the presence of such entity. Here we report a case of persistent ST-segment elevation due to a metastatic cardiac tumor.

Effect of Aortic Valve Opening Pattern on Endothelial Function After Continuous-Flow Left Ventricular Assist Device Implantation.

This study aimed to evaluate the effects of aortic valve opening patterns on endothelial functions in patients undergoing continuous-flow left ventricular assist device (CF-LVAD) implantation. This study included 43 patients who underwent CF-LVAD implantation and 35 patients with heart failure reduced ejection fraction (HFrEF; control group). The CF-LVAD group was divided into three subgroups based on aortic valve opening patterns: open with each beat, intermittently opening, and not opening groups. Flow-mediated dilatation (FMD) and pulsatility index (PI) were compared before and 3 months after CF-LVAD implantation. Cardiopulmonary exercise test (CPET) and 6 minute walk test (6-MWT) scores were measured at baseline and follow-up in the CF-LVAD group. The mean FMD and PI of patients in the CF-LVAD group reduced 3 months after implantation. Patients with intermittently opening and not opening aortic valves had worse endothelial function at follow-up. Before and 3 months after implantation FMD% did not significantly differ in patients whose aortic valves were open with each beat (4.72 ± 1.06% vs. 4.67 ± 1.16%, p = 0.135). Pulsatility index changes paralleled FMD changes. Cardiopulmonary exercise test and 6-MWT scores improved after implantation but without significant differences between subgroups. Maintaining normal aortic valve function after CF-LVAD implantation may reduce endothelial dysfunction; however, larger studies are needed for long-term clinical effects.

Effects of Continuous-Flow Left Ventricular Assist Device Therapy on Peripheral Vascular Function.

The peripheral vascular effects of continuous-flow left ventricular assist device (CF-LVAD) implantation are still unclear. The aim of the current study was to determine peripheral vascular function before and after implantation of CF-LVAD in patients with end-stage heart failure (HF), and to compare this data to age- and sex-matched chronic heart failure with reduced ejection fraction (HFrEF) patients. Forty-three consecutive end-stage HF patients (New York Heart Association [NYHA] class III/IV; three women and 40 men; mean age 53 ± 11 years) who planned to receive CF-LVAD implantation comprised the LVAD patient population, and their clinical characteristics, preoperative and third postoperative month peripheral vascular function assessment data including flow-mediated dilation (FMD) and pulsatility index (PI) assessed by ultrasound Doppler in brachial artery were compared to age- and sex-matched chronic, stable HFrEF patients (NYHA class II; five women and 30 men; mean age 51 ± 10 years). After CF-LVAD implantation, median FMD decreased from 5.4 to 3.7% (p < 0.001), and median PI decreased from 6.9 to 1.4 (p < 0.001). In patients with end-stage HF before CF-LVAD implantation, FMD and PI were significantly lower compared to the chronic HFrEF patients (FMD: 5.4% ± 0.9% vs. 7.6% ± 1.1%; p < 0.001, respectively) and (PI: 6.9 ± 1.3 vs. 7.4 ± 1.2; p = 0.023, respectively). The current study revealed impaired peripheral vascular function in the end-stage HF patients compared to stable HFrEF patients, and documented the deterioration of peripheral vascular function after CF-LVAD implantation. These results suggest that impaired peripheral vascular function in the CF-LVAD patients compared to preoperative assessment is a consequence of the nonpulsatile blood flow due to the continuous-flow mechanical support.

Characteristics and long-term survival of patients with left ventricular non-compaction cardiomyopathy.

AIMS: Left ventricular non-compaction cardiomyopathy (LVNC) is a poorly understood entity resulting in heart failure. Whether it is a distinct form of cardiomyopathy or an anatomical phenotype is a subject of discussion. The current diagnosis is based on morphologic findings by comparing the compacted to non-compacted myocardium. The study aimed to compare demographic and prognostic variables of patients with dilated cardiomyopathy (DCM) and LVNC. Emphasis was given to cardiac magnetic resonance (CMR) imaging analysis. Data on survival were also assessed. METHODS AND RESULTS: We retrospectively evaluated the characteristics and outcomes of 262 non-ischaemic cardiomyopathy patients with LVNC and DCM phenotypes. Petersen's CMR criteria of non-compacted to the compacted myocardial ratio 2.3 were used to diagnose LVNC. The primary endpoint was a composite endpoint of major adverse cardiovascular events comprising cardiovascular-related death, left ventricular assisted device implantation, or heart transplantation. A total of 262 patients with CMR data were included in the study. One hundred fifty-five patients who fulfilled CMR criteria were diagnosed as LVNC. CMR findings revealed that LVNC patients had higher left ventricular end-diastolic (137.2 ± 51.6, 116.8 ± 44.6, P = 0.002) and systolic volume index (98.4 ± 49.5, 85.9 ± 42.7, P = 0.049). Cardiac haemodynamics, cardiac output (5.61 ± 2.03, 4.96 ± 1.83; P = 0.010), stroke volume (73.9 ± 28.8, 65.1 ± 25.1; P = 0.013), and cardiac index (2.85 ± 1.0, 2.37 ± 0.72; P < 0.0001), were higher in LVNC patients. Of all the 249 patients, 102 (40.9%) patients demonstrated late gadolinium enhancement (LGE). According to Petersen's criteria, the Kaplan-Meier survival outcome did not reveal significant differences (hazard ratio [HR]: 1.53, 95% confidence interval [CI]: [0.89-2.63], P = 0.11). The presence or pattern of LGE did not show significant importance for endpoint-free survival. Most of the sub-epicardial LGE pattern was found in LVNC patients (94.4%). When receiver operator characteristics analysis was applied to NC/C ratio to discriminate the primary endpoint, a higher NC/C ratio of 2.57 was associated with adverse events (HR: 1.90, 95% CI: [1.12-3.24], P = 0.016). CONCLUSIONS: Our study questions the criteria being used for the diagnosis of LVNC. Further evaluation of CMR variables and association of these findings with demographic variables and survival is mandatory.

Comparison of ischemic side effects of levosimendan and dobutamine with integrated backscatter analysis.

BACKGROUND: Levosimendan improves cardiac contractility without increasing oxygen consumption. However, its effects on ischemia were not supported with the utilization of a noninvasive parameter of myocardial characterization. HYPOTHESIS: The changes observed in integrated backscatter (IBS) may be reflective of change in myocardial ischemia. In this study, the effect of levosimendan on ischemia detected by IBS was evaluated in patients with ischemic heart failure (HF). METHODS: Patients who had LVEF < 40% and NYHA III-IV symptoms of HF were included in this study. Patients were randomized to levosimendan (n = 21), or to dobutamine (n = 25) groups. The cyclic variation of integrated backscatter (CVIBS) was determined as the difference between the maximal and minimal values in a cardiac cycle, average of three consecutive beats. CVIBS was taken from the mid-anteroseptal, mid-inferior, and mid-posterolateral areas of the parasternal short axis images before the drug administration and at the end of the 24-hour infusion period. RESULTS: Baseline characteristics and concomitant medications were similar in both groups. A significant reduction in CVIBS was detected in anteroseptal (7.6 +/- 1.4 dB versus 5.9 +/- 0.8 dB, p = 0.01), inferior wall (7.4 +/- 0.8 dB versus 6.7 +/- 1.5 dB, p = 0.03), and posterolateral wall (9.0 +/- 1.2 dB versus 8.2 +/- 0.6 dB, p = 0.04) after dobutamine administration, while no significant changes were observed in the levosimendan group in all walls. CONCLUSIONS: Unlike dobutamine, levosimendan may not induce myocardial ischemia as shown by CVIBS at commonly used dosages in the setting of decompensated HF without active ischemia.

The role of tilt training in preventing recurrent syncope in patients with vasovagal syncope: a prospective and randomized study.

BACKGROUND: Recurrent vasovagal syncope (VVS) can be a severely disabling disorder that may lead to an important deterioration of quality of life because of the severity and recurrence of episodes. This study sought to investigate the effectiveness of repeated orthostatic self-training in preventing syncope in patients with recurrent VVS. METHODS: Eighty-two consecutive patients (mean age 41 +/- 4 years, 37 males) with recurrent VVS episodes and positive head-up tilt testing (HUT) were enrolled in this study. The patients were then randomized (1:1) to conventional therapy or conventional therapy plus additional tilt training sessions. The patients were followed for spontaneous syncope for one year. Primary end-points were the recurrence of syncope, the number of episodes, and the interval of time to the first recurrence. RESULTS: There were no significant differences of baseline clinical characteristics and parameters of HUT between the tilt training and control groups. The patients had 4 +/- 2/year syncopal episodes prior to the HUT. The mean follow-up after randomization was 12 +/- 2 months. Spontaneous syncope recurrence during follow-up was 56% (23 patients) versus 37% (15 patients) in the control and tilt training groups, respectively (P = 0.1). Time to first recurrence was also similar in both groups (70 +/- 20 days vs 50 +/- 15 days, P = 0.09). The frequency of recurrent syncopes was similar in all types of VVSs while the rate of episodes was significantly higher in control group in patients with vasodepressor type during follow-up period (32% vs 10%, P = 0.04). The mean number of recurrent syncope episodes was also similar in both groups (3 +/- 1 vs 2 +/- 1, P = 0.4). CONCLUSIONS: Tilt training was unable to influence the spontaneous syncope recurrence for recurrent VVS except for vasodepressor type.

Circadian and infradian rhythms of vasovagal syncope in young and middle-aged subjects.

BACKGROUND: The most cardiovascular physiological and pathophysiological events show a circadian rhythm. It is thought that the autonomic nervous system and biologic factors play a key role in the pathogenesis of vasovagal syncope (VVS). In this study, we investigated the circadian and infradian variation of VVS. METHODS: A prospective consecutive series of 246 patients (142 women; mean age 36+/-7 years) with recurrent syncope and with a positive head-up tilt testing (HUT) were included in this study. The daily and weekly distributions of the syncopal episodes were investigated. The assessments of episodes were done according to the days of the week and three time periods of the day (6 a.m.-12 noon, 12 noon-6 p.m., 6 pm-12 midnight). RESULTS: According to the results of HUT, 76 patients (31%) had cardioinhibitory, 62 patients (25%) had vasodepressor, and 108 patients (44%) had mixed type of VVS. During the initial passive phase, 40% of patients (99/246) showed positive response. Time to syncope was 20+/-2 minutes during HUT. The mean number of syncopal episodes was 4+/-2/years. In all, 1,070 episodes were evaluated. The distribution of the episodes in 6-hour intervals was significantly different from uniform occurrence (38%, 33%, and 29%, respectively) (P=0.02). The frequency of episodes was higher in the morning (P=0.045) and in the middle of the week (P=0.046). A significant difference was found between week and weekend days in terms of the frequency of episodes (75.5% vs 24.5%, P=0.01). CONCLUSION: VVS may show a circadian and infradian rhythm.

Effects of levosimendan on left atrial functions in patients with ischemic heart failure.

BACKGROUND: With further progression of left ventricular (LV) dysfunction, the left atrial (LA) contribution to LV filling gradually decreases, and LA dysfunction deteriorates the decreased LV filling in patients with heart failure (HF). HYPOTHESIS: This study sought to investigate the effects of levosimendan on LA function in patients with HF. METHODS: A total of 60 patients having acute decompensated HF with ischemic cardiomyopathy and LV ejection fraction (LVEF) < 40% were included in the study. Patients were randomized to levosimendan (n = 30) or to dobutamine (n = 30). Before and 24 h after treatment, LVEF, mitral inflow peak E and A wave velocity, E/A ratio, mitral lateral annulus peak Em wave velocity, E/Em ratio, LA volumes, and from the LA volumes the active emptying fraction (AEF), passive emptying fraction (PEF), and reservoir fraction (RF) were measured. RESULTS: All LA volumes were significantly reduced after levosimendan administration, but in the dobutamine group only minimal volume (Vmin) was reduced. Although AEF increased in both groups, the improvement of AEF was greater in the levosimendan group than in the dobutamine group (14% +/- 9% versus 2% +/- 1%, p = 0.001). The PEF (12% +/- 8% versus 21% +/- 6%, p = 0.04) and RF (23% +/- 4% versus 38% +/- 3%, p = 0.001) significantly increased after levosimendan administration, whereas these parameters did not change after dobutamine. In patients receiving levosimendan, there was a significant, positive correlation between PEF and Em (r = 0.475, p = 0.008), and there were significant negative correlations between PEF and E/Em (r = - 0.491, p = 0.006), and AEF and E/Em (r = - 0.654, p = 0.001). CONCLUSIONS: Left atrial functions respond better to levosimendan than to dobutamine in decompensated HF.

Primary cardiac amyloidosis mimicking interstitial lung disease and bleeding diathesis: a case report.

Primary amyloidosis is a rare systemic disease due to various organ involvements that can lead to atypical clinical findings. In this article, we discuss a case of primary cardiac amyloidosis in a patient presenting with bleeding eyelids and interstitial lung disease.

Myocardial bridge: a bridge to atherosclerosis.

OBJECTIVE: Myocardial bridge (MB) is a congenital anomaly characterized by narrowing during systole of some of the epicardial coronary arterial segments running in the myocardium. Although, it is considered as a benign anomaly, it may lead to such complications as acute myocardial infarction, ventricular tachycardia, syncope, atrioventricular block and sudden cardiac death. In this study, we aimed to investigate demographic, clinical and angiographic characteristics of the patients with MB found on coronary angiography. METHODS: The present study included 71 patients with MB found on coronary angiographies performed in our institution between January 1999 and September 2003. Based on the findings on angiography, the patients were subdivided into group A (n=41) and group B (n=30). The patients in the group A had no atherosclerotic lesion and the patients in the group B had coronary artery disease in addition to MB. Angiographic, demographic and clinical characteristics of both groups were compared. RESULTS: There were no differences between two groups in distribution of gender and risk factors of coronary artery disease whereas mean age of the patients in the group A was lower (47+/-5 years vs 55+/-11 years, p=0.01). Frequency of two or more risk factors for coronary artery disease in a particular patient was significantly higher in the group B (55% vs 30%, p=0.03). Myocardial bridge was located at proximal or mid segments of left anterior descending artery (LAD) in 40 patients whereas its presence in both LAD and right coronary artery was found only in one patient in group A. Mean bridging percent was 43+/-27% in group A. Localization of MB was LAD in 29 patients of group B. One patient with severe aortic valve stenosis in this group had MB at first septal branch. Mean bridging percent was 70+/-25% in group B, which was significantly higher than in group A (p<0.05). Atherosclerotic narrowing developed in only LAD in 14 patients, LAD and other vessels in 7 patients and in the vessels without MB in 9 patients. In patients with MB in LAD atherosclerotic narrowing of vessel developed proximally to the MB. Clinically, stable angina pectoris was seen more frequently in group A than group B (70% vs 35%, p=0.01), whereas the frequency of acute coronary syndrome was higher in group B (65% vs 30%, p=0.04). In regard to therapeutic approach, more patients in the group A received medical management (80% vs 50%, p=0.01), while more patients in the group B underwent surgical and percutaneous interventions (50% vs 18%, p=0.04). CONCLUSION: Myocardial bridge probability should be considered in young patients presenting with angina or if the same symptoms are persistent in the patients without more than one risk factor for coronary artery disease. Myocardial bridge may initiate the development of atherosclerotic lesion or may facilitate progression of atherosclerosis in the proximal segment of the vessel. The risk of acute coronary syndrome rises when atherosclerosis is superimposed on MB. Myocardial bridge should be considered in the young patients, presenting with angina or its equivalents without atherosclerotic lesions on coronary angiography.

Characteristics of periodontal microflora in acute myocardial infarction.

BACKGROUND: Periodontitis has been linked to increased risk of cardiovascular diseases. Systemic reactions associated with cardiovascular events may depend on characteristics of the subgingival microflora in periodontitis. Our objectives were to compare the numbers of cultivable bacteria, composition of subgingival microflora and clonal distribution of Actinobacillus actinomycetemcomitans (A. actinomycetemcomitans) in two groups of patients with generalized chronic periodontitis (GCP), one with an acute myocardial infarction (AMI-GCP) and the other one without AMI (non-AMI-GCP). METHODS: In all, 150 dentate individuals were screened for suitability to this study. Subgingival bacterial samples were collected from 11 AMI-GCP and 11 non-AMI-GCP patients who had been selected using strict inclusion criteria in an attempt to exclude confounding factors and to increase comparability of periodontal conditions by matching for periodontal probing depths and attachment levels. Culture methods were used to determine the total viable counts and occurrence and proportions of six periodontal bacterial species and yeasts. Polymerase chain reaction (PCR) technique was used to detect A. actinomycetemcomitans and Porphyromonas gingivalis (P. gingivalis). Intraspecies characterization of A. actinomycetemcomitans included serotyping and genotyping. RESULTS: The mean proportions of P. gingivalis (P = 0.05) and Tannerella forsythensis (T. forsythensis) (P = 0.01) were significantly lower, but the numbers of Micromonas micros (M. micros) and A. actinomycetemcomitans were up to nine times higher and the mean total number of cultivable bacteria per sample higher (P <0.01) in AMI-GCP than in non-AMI-GCP. CONCLUSION: The findings that no target subgingival species were overrepresented but the total bacterial number was higher in AMI-GCP than non-AMI-GCP patients may provide support to the hypothesis that elevated numbers of bacteria in close vicinity to sterile parenteral area present a risk for systemic health.

Successful balloon angioplasty of native aortic coarctation in a young adult with refractory hypertension.

Controversy exists with regard to the role of balloon angioplasty in the treatment of native aortic coarctation. Recent data and studies have showed that percutaneous balloon angioplasty is a safe and effective treatment for aortic coarctation. We report a young adult with aortic coarctation who has been treated with successful balloon angioplasty.

Decreased soluble cell adhesion molecules after tirofiban infusion in patients with unstable angina pectoris.

AIM: The inflammatory response, initiated by neutrophil and monocyte adhesion to endothelial cells, is important in the pathogenesis of acute coronary syndromes. Platelets play an important role in inflammatory process by interacting with monocytes and neutrophils. In this study, we investigated the effect of tirofiban on the levels of cell adhesion molecules (soluble intercellular adhesion molecule-1, sICAM-1, and vascular cell adhesion molecule-1, sVCAM-1) in patients with unstable angina pectoris (AP). METHODS: Thirty-five patients with unstable AP (Group I), ten patients with stable AP (Group II) and ten subjects who had angiographycally normal coronary arteries (Group III) were included the study. Group I was divided into two subgroups for the specific treatment regimens: Group IA (n = 15) received tirofiban and Group IB (n = 20) did not. Blood samples for investigating the cell adhesion molecules were drawn at zero time (baseline; 0 h) in all patients and at 72 h in Group I. RESULTS: The baseline levels of sICAM-1 and sVCAM-1 were higher in Group I than in Groups II and III. They were higher in Group IA than in Group IB. However, the sICAM-1 and sVCAM-1 levels decreased significantly in Group IA after tirofiban infusion. In contrast, these levels remained unchanged or were increased above the baseline value in Group IB at 72 h. CONCLUSION: The levels of cell adhesion molecules in patients with unstable AP decreased significantly after tirofiban infusion. Inhibition of platelet function by specific glycoprotein IIb/IIIa antagonists may decrease platelet-mediated inflammation and the ischemic end-point.

QT dispersion in patients with different etiologies of left ventricular hypertrophy: the significance of QT dispersion in endurance athletes.

Left ventricular hypertrophy (LVH) increases the risk of ventricular arrhythmias and sudden death and has a significant effect on total cardiovascular mortality. QT dispersion (QTd) is a measure of inhomogeneous repolarization and is used as an indicator of arrhythmogenicity. In this study we detected QTd in patients with different etiologies of left ventricular hypertrophy and the effect of LVH in QTd on endurance athletes. The study group consisted of 147 white male subjects with 3 different etiologies of LVH and 30 healthy male individuals. The underlying etiologies of LVH were essential hypertension, valvular aortic stenosis and long-term training (athletic heart). QTd was measured by surface electrocardiogram and Bazett's formula was used to correct QTd for heart rate (QTcd). Left ventricular mass was determined by transthoracic echocardiography and left ventricular mass index was calculated in relation to body surface area. The QTcd was significantly higher in patients with pathological LVH (due to hypertension and aortic stenosis) than in the athletes' group (physiological LVH) and healthy subjects (P<0.05). The magnitude of QTcd was similar between athletes and the control group (P=0.6). The difference of QTcd between the groups with pathological LVH was not statistically significant (P=0.1). In conclusion; the increasing of QT dispersion is associated with only pathological conditions of LVH. The left ventricular hypertrophy has not a negative effect in QT dispersion on endurance athletes. The measurement of QT dispersion may be a non-invasive useful method for screening additional pathological conditions in endurance athletes.

The angiographic correlation between ST segment depression in noninfarcted leads and the extent of coronary artery disease in patients with acute inferior myocardial infarction: a clue for multivessel disease.

BACKGROUND: Although reciprocal ST segment depression (RSTD) in patients with acute inferior myocardial infarction is a common electrocardiogram finding, its significance is not yet established. In this prospective study, the relationship between RSTD and the extent of coronary artery disease (CAD) was investigated. PATIENTS AND METHODS: One hundred eighty-eight patients with acute inferior myocardial infarction who received thrombolytic therapy were enrolled in this study. The magnitude and location of ST segment depression in noninfarcted leads and the maximum ST segment elevation (STEmax) in inferior leads were measured. All patients were divided into two main groups according to the presence of RSTD and five subgroups according to the location of RSTD, the maximum RSTD and the STEmax. The coronary angiography was performed in all patients 28 +/- 4 days after acute myocardial infarction. RESULTS: There were no significant differences in the proportion of coronary disease risk factors in patients with, versus those without, RSTD (P=0.6). Multivessel CAD was present in 63 of the 108 (58%) patients with RSTD and in 32 of the 80 (40%) patients with no RSTD (P=0.02). According to the location of reciprocal changes, multivessel disease was present in significantly more patients with anterior RSTD concomitant with or without lateral ST segment depression (P=0.01 and P=0.03, respectively); the proportion of single vessel disease was greater in patients with only lateral RSTD (P=0.02). In addition, the presence of anterior RSTD to a greater magnitude than the STEmax in inferior myocardial infarction increases the likelihood of multivessel disease (P=0.006). CONCLUSIONS: The presence of RSTD during an acute inferior myocardial infarction correlates with the presence of multivessel CAD and may not be only an electrical phenomenon.

The predictive value of mitral leaflet motion and thickness index scores on early restenosis after mitral balloon valvuloplasty.

The purpose of this study was to investigate whether there is any association between mitral leaflet motion (LMI) and leaflet thickness index (LTI) scores and the rate of restenosis 3 months after successful mitral balloon valvuloplasty. The study population consisted of 46 patients with symptomatic rheumatic mitral stenosis who underwent balloon valvuloplasty (37 women, 9 men; mean age, 36 +/- 9 years). Two-dimensional and Doppler echocardiography were performed in all patients on the day before, immediately after, and 3 months after valvuloplasty. The severity of restriction of leaflet motion and the severity of leaflet thickening were classified into grades of mild (a score of 0), moderate (a score of 1), and severe (a score of 2). Subvalvular disease and commissural involvement were homogeneous in all patients. Before and immediately after mitral balloon valvuloplasty, there were no significant differences in mitral valve area among the groups with different LMI and LTI scores. However, at 3 months after valvuloplasty, reduction in mitral valve area was more significant in patients who had higher pre-procedural LMI and LTI scores (P < 0.05). The rates of early restenosis were 0 with a total score of 0, 14.2% with a total score of 1-2, and 32% with a total score of 3. In conclusion, quantitative assessment of LMI and LTI scores by 2-dimensional echocardiography may be helpful in predicting early restenosis after mitral balloon valvuloplasty. Early reduction in mitral valve area is significant in patients who have higher total LMI and LTI scores.

[Effects of metoprolol on the signal averaged electrocardiogram and QT dispersion in acute myocardial infarction]. / Akut miyokard infarktüsünde metoprolol'ün sinyal ortalamali elektrokardiyogram ve QT dispersiyonu uzerine etkisi.

OBJECTIVE: The determination of high risk patients for sudden death and sustained ventricular tachycardia after acute myocardial infarction constitutes the main goal to decrease morbidity and mortality. Every attempt that decreases the frequency of late potentials (LPs) on signal averaged ECG (SAECG) and corrected QT dispersion (QTc-d) may improve prognosis of patients. In this study, the effect of metoprolol on frequency of LPs and QTc-d was investigated. METHODS: Thirty-five patients (mean age 53 +/- 9 years) with acute myocardial infarction who were not given thrombolytic therapy were enrolled. Patients in whom metoprolol was not administered formed group I (n = 20) and patients who were given metoprolol constituted group II (n = 15). Metoprolol was administered as an initial dose of 15 mg intravenously, following 6-8 hours 100 mg/d orally. To determine the frequency of LPs, SAECG records were performed on admission and at the end of the first week. At the same time, resting ECG recordings (12 leads, 50 mm/s) were obtained to calculate QTc-d. Variance analysis was used for statistical analysis. RESULTS: In group I; frequency of LPs were found 30% on admission and at the end of the first week. In group II; frequency of LPs were 6% on admission and at the end of the first week there was no LPs. There was no statistically significant difference between two groups according to TQRS, RMS-40, LAS40 and QTc-d CONCLUSION: Metoprolol decreases the frequency of LPs. It has no effect on cQT-d.

Is a drug-challenge test with propafenone adequate to exclude Brugada syndrome?

Brugada syndrome is associated with sudden cardiac death in patients with a structurally normal heart. The electrocardiogram (ECG) pattern of Brugada syndrome is characterised by complete or incomplete right bundle branch block and ST-segment elevation in the right precordial leads. These ECG signs may not always be apparent but can be unmasked with certain anti-arrhythmia agents. We report here a case of a 26-year-old woman without detectable structural heart disease but with a history of syncope, cardiac arrest, intubation and defibrillation for ventricular fibrillation. We performed challenge tests with propafenone and ajmaline. After infusion of propafenone, there were minimal ECG changes which were not diagnostic for Brugada syndrome. One week later the provocation test was repeated with ajmaline. During infusion of ajmaline, prominent J waves and ST-segment elevation appeared in the right precordial leads (V1-3). Premature ventricular complexes were seen on a 12-lead ECG. The patient's ECG showed Brugada type 1 pattern. She received an internal cardioverter/defibrillator and was discharged with a beta-blocker.

Acute myocardial infarction is reflected in salivary matrix metalloproteinase-8 activation level.

BACKGROUND: The aim of this study is to compare salivary and serum biomarker levels and degrees of matrix metalloproteinase (MMP) activation between patients with acute myocardial infarction (AMI) and systemically healthy patients (non-AMI) with similar periodontal conditions. METHODS: A total of 92 patients (47 AMI and 28 non-AMI patients with gingivitis or periodontitis; and 17 systemically and periodontally healthy patients as a control group) were recruited. Clinical periodontal measurements were recorded; stimulated whole saliva and serum samples were collected. AMI patients were clinically examined within 3 to 4 days after admission to the coronary care unit. Saliva samples were analyzed for levels of MMP-8, MMP-7, and tissue inhibitor of matrix metalloproteinase (TIMP)-1. Serums were tested for MMP-8, MMP-9, TIMP-1, and TIMP-2 levels by immunofluorometric assay and enzyme-linked immunosorbent assay. Molecular forms and degree of activation of salivary MMP-8, MMP-9, and MMP-13 were analyzed by computer-scanned immunoblots. RESULTS: Total salivary MMP-8 assessed by immunofluorometric assay method and immunoblot densitometric units was higher in non-AMI than in AMI patients' saliva, but a significantly higher percentage of AMI patients' MMP-8 was activated polymorphonuclear leukocyte (PMN) type (P <0.001) regardless of periodontal diagnosis.Serum MMP-8, MMP-9, and TIMP-1 levels were significantly higher in AMI (for all markers and all comparisons,P <0.05). Characteristic for AMI was dominance of active PMN MMP-8 in saliva [corrected].