V1与V3R～V6R导联QRS波群相关性分析

目的探讨右胸导联正常QRS波群的内在规律。方法观察220例健康大学生常规12导联和V3R-V6R导联心电图，分析V1QRS波群呈不同形态时V3R-V6R导联QRS形态和q波时间、电压及q／R比值。结果V3R-V6R与V1QRS形态相似率逐导联降低；V3R-V6Rq及Qs波出现率逐导联增高（1．82％、6．82％、23．64％、47．27％）；V1呈Rs时V3R、V4R无q或QS波，V1呈QS时V3R、V4R均呈QS型；V3R、V4R或V5R出现q或QS波，则其右侧导联也出现q或QS波（即不会单个导联出现q或QS波）；V3R-V6Rq波时间〈0．04s，q／R比值可〉1／4。结论正常人右胸导联可出现q或QS波，孤立导联的q或QS波有临床意义。     

S‐R difference in V1‐V2 is a novel criterion for differentiating the left from right ventricular outflow tract arrhythmias

Aim

The correct estimation of the VA origin as RVOT or LVOT results in reduced ablation duration reduced radiation exposure and decreased number of vascular access. In our study, we aimed to detect the predictive value of S‐R difference in V1‐V2 for differentiating the left from right ventricular outflow tract arrhythmias.

Methods

We included 123 patients with symptomatic frequent premature ventricular outflow tract contractions who underwent successful catheter ablation (70 male, 53 female; mean age 46.2 ± 13.9 years, 61 RVOT, 62 LVOT origins). S‐R difference in V1‐V2 was calculated with this formula on the 12‐lead surface ECG: (V1S + V2S) – (V1R + V2R). Conventional ablation was performed in 101 (82.1%) patients, CARTO electroanatomic mapping system was used in 22 (17.9%) patients.

Results

V1‐2 SRd was found to be significantly lower for LVOT origins than RVOT origins (p < .001). The cutoff value of V1‐2 SRd obtained by ROC curve analysis was 1.625 mV for prediction of RVOT origin (sensitivity: 95.1%, specificity: 85.5%, positive predictive value: 86.5%, negative predictive value: 94.5%). The area under the curve (AUC) was 0.929 (p < .001).

Conclusion

S‐R difference in V1‐V2 is a novel and simple electrocardiographic criterion for accurately differentiating RVOT from LVOT sites of ventricular arrhythmia origins. The use of this simple ECG measurement could improve the accuracy of OTVA localization, could be beneficial for decreasing ablation duration and radiation exposure. Further studies with larger patient population are needed to verify the results of this study.

     

Significance of ST-Segment elevation in V4R lead in patients with anterior myocardial infarction

Background

There is some evidence of the association between ST-segment elevation in the V4R chest lead and the likelihood of anterior wall myocardial infarction; however, the link of this phenomenon with the location and the severity of the coronary involvements in such patients remains uncertain. We aimed to investigate the ST-segment elevation in V4R leads in patients with anterior myocardial infarction and also its effect on prognosis as well as the detection and prediction of the location of arterial stenosis in coronary angiography.

Methods

Data collection was performed by reviewing the hospital recorded files of 195 patients’ suspicion of acute myocardial infarction who have been referred within 2 h of the onset of cardiac symptoms. The patients were then categorized into two groups with and without ST elevation in the V4R chest lead.

Results

Comparing two groups showed a significantly higher rate of concurrent ST-segment elevation in V₁ lead in those with ST-segment elevation in V4R. Echocardiography on the day after anterior myocardial infarction showed LVEF <40% in 74% and 35.2% of patients with and without ST-segment elevation in V4R, respectively, indicating a significant difference. The lesions on proximal LAD were more common in the group with ST-segment elevation in V4R.

Conclusion

Our study emphasized a high likelihood of ST-segment elevation in V4R lead concurrently with ST-elevation in V₁ lead. Also, the appearance of ST-segment elevation in V4R lead can be accompanied with a lower LVEF, myocardial infarct size, involvement of proximal part of LAD, and Wrap around LAD.

     

A highly polymorphic microsatellite in the factor V gene is an informative tool for the study of factor V-related disorders

The role of factor V (FV) mutations in activated protein C (APC) resistance and FV deficiency is well established. We report on the identification of a highly polymorphic (AT)n microsatellite marker in the FV gene, which represents an informative tool for the investigation of the origin and evolution of pathologically relevant FV genetic components. A high number of different microsatellite alleles were found to be associated with FV R506Q and FV H1299R, two single-origin mutations. An example of the use of the microsatellite marker in family studies of thrombophilia and FV deficiency is also provided.     

Significance of ST‐Segment elevation in V4R lead in patients with anterior myocardial infarction

BackgroundThere is some evidence of the association between ST‐segment elevation in the V4R chest lead and the likelihood of anterior wall myocardial infarction; however, the link of this phenomenon with the location and the severity of the coronary involvements in such patients remains uncertain. We aimed to investigate the ST‐segment elevation in V4R leads in patients with anterior myocardial infarction and also its effect on prognosis as well as the detection and prediction of the location of arterial stenosis in coronary angiography.MethodsData collection was performed by reviewing the hospital recorded files of 195 patients’ suspicion of acute myocardial infarction who have been referred within 2 h of the onset of cardiac symptoms. The patients were then categorized into two groups with and without ST elevation in the V4R chest lead.ResultsComparing two groups showed a significantly higher rate of concurrent ST‐segment elevation in V₁ lead in those with ST‐segment elevation in V4R. Echocardiography on the day after anterior myocardial infarction showed LVEF <40% in 74% and 35.2% of patients with and without ST‐segment elevation in V4R, respectively, indicating a significant difference. The lesions on proximal LAD were more common in the group with ST‐segment elevation in V4R.ConclusionOur study emphasized a high likelihood of ST‐segment elevation in V4R lead concurrently with ST‐elevation in V₁ lead. Also, the appearance of ST‐segment elevation in V4R lead can be accompanied with a lower LVEF, myocardial infarct size, involvement of proximal part of LAD, and Wrap around LAD.     

正常人V2导联R/S＞1的心电图分析

目的探讨正常人心电图单纯出现V2导联R/S>1的发生情况。方法随机抽取健康体检中正常人3987名(男性2108名,女性1879名,年龄范围20～60岁),常规心电图检出V2导联R/S>1共计349名(男性206名,女性143名),按性别分男、女2组,按年龄分为4个年龄组,并对V2导联的R波及V6导联的q波的波形、振幅及时限进行分析。结果正常的健康人群中9.8%男性和7.6%女性出现V2导联R/S>1。40～50岁的年龄组最高,达10.2%。95.1%V2导联R波时限在0.4～0.5s。V6导联无q波或有q波时限均<0.02s,93.4%振幅<0.10mV。结论V2导联作为移行区导联出现R/S>1现象较常见,考虑为生理性改变。     

New Electrocardiographic Features in Brugada Syndrome

Brugada syndrome is a genetically determined familial disease with autosomal dominant transmission and variable penetrance, conferring a predisposition to sudden cardiac death due to ventricular arrhythmias. The syndrome is characterized by a typical electrocardiographic pattern in the right precordial leads. This article will focus on the new electrocardiographic features recently agreed on by expert consensus helping to identify this infequent electrocardiographic pattern.     

A case of factor V inhibitor

A 57-year-old married Chinese male without a family history of bleeding disorder was presented with severe hemorrhagic tendency and was subsequently found to be suffering from an acquired inhibitor against coagulation factor V. The prolonged prothrombin time and activated partial thromboplastin time could not be corrected by the addition of normal plasma. Subnormal value of factor V level was noted accompanied with an abnormal platelet factor III availability test. With specific antisera and staphylococcal protein A, the inhibitor was characterized as an IgG(lambda) antibody. The hemorrhagic tendency and abnormal laboratory data were corrected after treating the patient with platelet concentrate transfusion and cyclophosphamide.     

R255h amino acid substitution of protein Z identified in patients with factor V Leiden mutation

The clinical significance of diminished protein Z in plasma is controversial. Studies in mice demonstrated that deficiency of protein Z dramatically increases the prothrombotic tendency of factor V Leiden mutation. This finding was confirmed by initial results in humans, indicating that thromboembolism in factor V Leiden patients with lowered protein Z level occurs earlier than in patients with normal protein Z levels. Consequently, the aim of our present study was to find out whether genetic alterations of protein Z were demonstrated in patients with factor V Leiden mutation and early onset of thromboembolic disease. DNA-sequencing of the protein Z gene was performed in two patients with factor V Leiden mutation, early onset of thromboembolism, and lowered protein Z levels. In both patients, R255H substitution of the protein Z gene was identified. Subsequently, the R255H substitution was also found in 12 of 132 additional patients. Patients presenting with the R255H substitution in addition to factor V Leiden mutation showed thromboembolic events more frequently than factor V Leiden patients without R255H substitution of the protein Z gene. In conclusion, R255H substitution of the protein Z gene seems to influence clinical symptoms of thromboembolism in factor V Leiden patients.     

Severe coagulation factor V deficiency caused by a 4 bp deletion in the factor V gene

Factor V (FV) deficiency (parahaemophilia) is an autosomal recessive bleeding disorder with an incidence of 1:10⁶. We have studied a young girl with very mild bleeding symptoms and undetectable levels of plasma factor V antigen and activity (<0.3% and <1.6% of normal, respectively). Both parents showed plasma levels of factor V activity of about 50% of normal. Sequence analysis of the 5'- and 3'-untranslated, coding and adjacent regions of the factor V gene revealed the presence of a 4 bp deletion in exon 13. Subsequent screening of members of the family for the mutation showed that both parents were heterozygous for the mutation, that one healthy sister carried only normal alleles, and that the patient was homozygous for the mutated allele. The mutation introduced a frameshift and a novel premature stop codon in codon 1303, and would predict the synthesis of a truncated factor V molecule that lacks part of the B domain and the complete light chain. However, no factor V heavy chain could be detected in the plasma of the patient. Furthermore, factor V activity could not be detected in the patients' platelets. This is the first reported mutation in the factor V gene that predicts a type I quantitative factor V deficiency. Surprisingly, the patient, who is homozygous for the mutation, so far has only a very mild bleeding tendency.     

Diagnostic and prognostic value of a type 1 Brugada electrocardiogram at higher (third or second) V1 to V2 recording in men with Brugada syndrome

To evaluate the diagnostic and prognostic value of an electrocardiogram (ECG) recorded at a higher (third or second) intercostal space, 98 men (17 to 76 years of age, mean +/- SD 47 +/- 13; with documented ventricular fibrillation [VF] in 22 and syncope in 32) were categorized into 3 groups; 68 men had a spontaneous type 1 ECG in standard leads V(1) and V(2) (S group), 19 had a spontaneous type 1 ECG only in the higher V(1) and V(2) leads (H group), and 11 had a type 1 ECG only after receiving class Ic sodium channel blockers (Ic group). There were no significant differences in baseline clinical characteristics, including VF episodes, syncope, atrial fibrillation, family history, late potentials, and inducibility of VF during electrophysiologic study across the 3 groups. During prospective follow-up periods (779 +/- 525, 442 +/- 282, and 573 +/- 382 days, respectively), subsequent cardiac events occurred in 11 men (16%) within the S group, in 2 men (11%) in the H group, and in 0 men (0%) in the Ic group (p = NS, S vs H group). In men with previous episodes of VF, subsequent cardiac events occurred in 7 (44%) within the S group and in 2 (50%) in the H group (p = NS). In conclusion, men with a spontaneous type 1 Brugada ECG recorded only at higher leads V(1) and V(2) showed a prognosis similar to that of men with a type 1 ECG in using standard leads V(1) and V(2).     

Factor V Q 506 mutation in children with thrombosis

The factor V Leiden mutation in 12 children with thrombosis and in 20 controls was investigated. Five heterozygous individuals and 1 homozygous individual among the cases with thrombosis and 1 heterozygous individual among controls were found. Central nervous system thromboses were increased in children with the factor V mutation, associated with protein S deficiency. © 1996 Wiley-Liss, Inc.     

Idiopathic factor V inhibitor in a patient starting haemodialysis

A 74-year-old Pacific Island man with end-stage renal failure planning to start haemodialysis presented with persistent bleeding after tunnelled dialysis catheter insertion. The laboratory findings revealed a prolonged activated partial thromboplastin time of 118 s, prothrombin ratio of 4.2, factor V activity of <2% and a factor V inhibitor of 40 Bethesda Units. No clear underlying aetiology was identified. The bleeding settled with conservative measures and the factor V inhibitor was successfully treated with oral cyclophosphamide for 6 weeks.     

Kt／V的测定方法、临床意义及其局限性

透析充分与否与维持性透析患者的生活质量和生存率密切相关.透析的主要目的之一是清除尿毒症毒素,使其维持在一定的水平.因此,毒素的清除是反映透析充分性的一个主要指标.     

Acquired Factor V Inhibitor Complicated with Immune Thrombocytopenia

We herein report a patient with a high bleeding tendency as a result of acquired factor V inhibitor and immune thrombocytopenia (ITP). The administration of prednisolone increased the platelet count, but a fatal bleeding event occurred before platelet levels had sufficiently increased. Factor V is stored in not only plasma but also platelets, and platelet-derived factor V might play a local hemostatic role. Bleeding tendency may be high in rare cases where factor V inhibitor is complicated with severe thrombocytopenia. In such patients, physicians should consider aggressive hemostatic therapy, including plasma exchange, in addition to immunosuppressive therapy.     

Electrocardiographic findings in leads V3R to V5R in patients with a slurred or notched S wave in lead V~

Background Right bundle branch block (RBBB) may present as slurred or notched S wave in lead V 1 . However, slurred or notched S wave may also represent slow conduction in the myocardium. Methods We retrospectively analyzed the QRS patterns in leads V3R to V5R in 7 patients with a slurred or notched S wave in lead V 1 . Results In the leads V 3R to V 5R , 6 patients showed incomplete or complete RBBB and 1 patient slurred or notched S wave. Conclusions In the majority of ECGs in a small patient series with slurred or notched S wave in lead V 1 , QRS morphology indicating incomplete or complete RBBB was present in leads V 3R to V 5R . A finding of fragmented QRS in these leads may indicate slow conduction in the myocardium.     

Combined factor V and VIII deficiency in Indian population

The clinical and haematological heterogeneity in cases of the rare combined factor V and VIII deficiency has not been reported so far from India. Nine such cases belonging to five unrelated families have been analysed in the present study for the various haematological and clinical parameters. A very mild clinical presentation is seen in all these cases. The clinical manifestations, however, do not correlate with the plasma levels of these factors.