Interruption of the Aortic Arch in the Adult and Fulminant Myocarditis: A Strange Presentation

Introduction

 
53 years old female patient, who presented oppressive precordial pain, radiating to the neck and jaw, for which she went to the emergency room, where an ECG image of complete left bundle branch block was evidenced (Figure 1), with taking ultrasensitive troponin I at > 50,000 pg/ml, presenting data of acute heart failure and acute pulmonary edema, requiring endotracheal intubation, moving urgently to cardiac catheterization without evidence of obstructive coronary lesions, observing in aortography interruption of the aortic arch with collateral vessels connecting to the descending aorta (Figure 2). Later in the ICU, an echocardiogram was performed that reported LVEF of 27%, generalized hypokinesia, severe MI and apical thrombus (Figure 3), diagnosing fulminant myocarditis, for which treatment with methylprednisolone at a dose of 500 mg for 3 days was started. presenting improvement with LVEF of 35%, however, she later presented septic shock of pulmonary origin, which led to the death of the patient. Aortic arch interruption is a congenital malformation characterized by complete interruption between the ascending and descending aorta, with 3 types according to the Celoria-Patton classification, B being the most frequent, while fulminant myocarditis is myocardial inflammation due to various etiologies , mainly viral, which can present from a picture of acute heart failure to cardiogenic shock and can simulate a picture of acute coronary syndrome. The importance of the previous case resides in the fact that, although there is no association between both pathologies, there is no case reported in the literature in which they occur simultaneously.

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Profile of Patients admitted with Hypertension at a Tertiary Level Hospital of Eastern Nepal

 

Abstract

Hypertension is a global public health issue that affects approximately 1 billion people worldwide in both developed and developing countries. It is also considered as an ‘Iceberg’ disease’ because unknown morbidity far exceeds the known morbidity. High blood pressure (BP) is ranked as the third most important risk factor for at attributable burden of disease in South Asia. With an aim to determine the profile of the hypertensive patients a retrospective cross-sectional study design was used to analyze the medical record of 1311 patients admitted with the primary diagnosis of hypertension at BPKIHS January 2005 to May 2016. The study revealed that majority (82.4%) of the patients was above 40 years of age with the mean age of 57.14 ±17.5. More than half (53.5%) of the patients were male. Almost half (49.4%) of the patients were from Sun sari district. More than 90% of the patients were admitted in medical ward. Majority (90.7%) of the patients were improved at the time of discharge.

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Lupine Publishers | MDCT in Diagnosis of Anomalies of Coronary Artery Origin and Course a Coronary MDCT-Angiographic study of 9572 patients

Lupine Publishers | Advancements in Cardiology Research & Reports

 

Abstract

Background: Coronary anomalies are the causes of sudden cardiac deaths in young peoples, but usually asymptomatic. We perform this retrospective study to determine the types and prevalence of Coronary Anomalies of origin and course.

Method: The data of 9572 patients with Coronary CT-angiography by MDCT 640 Aquilion Toshiba machine were analyzed.

Results: Anomalous origin and course of coronary artery were detected in 47 (0.49%) of 9572 patients. The anomalous origins of Circumflex Artery from the RCA or the right sinus of Valsalva are most frequently visualized ( 15 pts [31.9%] ). High taking off of RCA observed in 11 pts ( 23.4% ).The RCA rising from the left sinus of Valsalva were seen in 8 pts ( 17% ).The Left Coronary Artery originates from the right sinus of Valsalva in 5 pts ( 10,6% ).The RCA arising from the LAD in 2pts (4,2% ).Absent RCA in 2 case (4.2%) and single coronary artery from LSV in one case (2.1%). The LCA rising from the Pulmonary Artery ( ALCAPA) in 2 cases and The RCA originating from the PA in one case ( RCAPA ).

Conclusion: Anomalies of coronary artery origin and course are rare but the diagnosis is very important to prevent SCD in young patients. MDCT with the Volume Rendered Images is the non-invasive modality that provides the valuable information to detect these anomalies.

Keywords: Multidetector Computed Tomography; Anomalies of coronary origin and course; sinus of Valsalva

Introduction

Coronary artery anomalies are a diverse group of congenital heart diseases with manifestations and pathological mechanisms are highly variable. Coronary anomalies include anomalies of origin and course, anomalies of intrinsic coronary arterial anatomy like myocardial bridge, anatomy of coronary termination as coronary artery fistula and anomalous anastomotic vessels. Anomalies of coronary origin and course may associated with arrhythmias, myocardial infarction and sudden cardiac deaths in young people, especially on effort like athletes. We study 9572 patients with coronary MDCT-angiography to evaluate the type and the incidence of coronary anomalies of origin and course[1,2].

Methods

All patients who underwent coronary CT-angiography by MDCT 64O Aquilion Toshiba equipment ( IV contrast medium, gantry rotation of 0.33 msec, slice thickness 0.5mm ) in MEDIC HCMC Viet Nam, from January 2016 to January 2019 were included. The main indications of CT-angiography were acute coronary syndrome, stable angina, coronary CT-angiography prior to surgery, congenital heart diseases involving coronary artery...

The CT-angiograms with coronary anomalies were selected and analyzed. The anomalies of coronary origin and course were assessed [3-5].

Results

We included 9572 pts with anomalies of coronary origin and course based on results of CT-angiograms that were interpreted by two cardiologists. Anomalous origin and course of coronary artery were detected in 47 ( 0,49 %) of 9572 patients. The mean age of these pts was 63± 8.4, M/F=1.8 . The anomalous origins of Circumflex Artery from the RCA or the right sinus of Valsalva are most frequently visualized ( 15 pts [31.9%] ).High taking off of RCA observed in 11 pts ( 23.4% ) The RCA rising from the left sinus of Valsalva were seen in 8 pts ( 17% ).The Left Coronary Artery originates from the right sinus of Valsalva in 5 pts ( 10.6% ), in this subgroup, a patient presented by myocardial infarction resulting cardiac arrest was notified, the surgical re-implantation of LCA was performed .The RCA arising from the LAD in 2pts (4,2% ). Absent RCA in 2 case (4.2%) and single coronary artery from LSV in one case ( 2.1% ) (Table1 ).The Left Coronary Artery arising from the Pulmonary Artery ( ALCAPA ) in 2 cases ( 4.2% ) and The RCA originating from the PA ( RCAPA ) in one case ( 2.1% ). sinus of Valsalva (Figures 1-10).

Table 1.

RSV: Right sinus of Valsalva, LSV: Left sinus of Valsalva, ALCAPA: Anomalous Left Coronary Artery from The Pulmonary Artery, RCAPA: Anomalous Origin of the Right Coronary Artery off The Pulmonary Artery.

Figure 1: Single coronary artery rising from LSV.

This patient is of 52 ages, presented by atypical chest pain, the single coronary artery originating from LSV. The other case report of Prashanth Panduranga revealed the single coronary artery arising from RSV with exertional angina

Figure 2: High taking off of RCA.

Some time causes myocardial infarction due to excessive angulation between RCA and Aorta. We have in our study one young patient of 24 y.o that had been transferred to the hospital by cardiac arrest , related to this anomaly. Operative re-implanted had been indicated to save the patient

Figure 3: RCA originates from LSV with intra-arterial course resulting Angina

Figure 4: Anomalous origin of LCA from RSV

Figure 5: RCA rising from LSV and Intra-arterial course of RCA.

Figure 6:LCx arising from the RVS and Retro Aortic Course of LCx.

Figure 7: LCx arising from the RVS and Retro Aortic Course of LCx.

Figure 8: Anomalous Left Coronary Artery from The Pulmonary Artery.

Figure 9: Other case of ALCAPA.

Figure 10: Anomalous Origin of the Right Coronary Artery off The Pulmonary Artery.

Discussion & Conclusion

In our study, coronary anomalies of origin and course were detected in 47 of 9572 patients ( 0,49% ) that is consistent with the incidence of 0.27% to 1.66% reported in other series. The most frequent anomaly of origin and course was the Cx Artery arising from RCA/RSV ( 31.9% of anomaly prevalence and 0.16% among all patients ), this incidence is lower than previous published studies. The anomalies of origin and course of RCA were found in 17% and 4.2% respectively from LSV and LAD. This incidence is lower in comparison with previous study. Sudden deaths, myocardial infarction, arrhythmias related to the coronary anomalies were reported previously [6,7]. But these anomalies often asymptomatic, so early detection of coronary anomalies of origin and course is highly important. The former studies mainly based on the result of coronary angiography that is invasive modality. This study demonstrates MDCT is the noninvasive modality that provides important information related to coronary anatomy. Currently MDCT and MRI become fundamental to detection and diagnosis of coronary anomalies. Contrast enhanced ECG-gated 640-row MDCT coronary angiography is an accurate diagnostic method that can precisely detect the coronary anomalies of origin and course.

 

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Lupine Publishers | Platelets and Patent Ductus Arteriosus: Is there a Any Association Really?

Lupine Publishers | Advancements in Cardiology Research & Reports

 

 

Abstract

 

Introduction: A great number of the studies have shown that platelets play a role in closure of the PDA. However, studies that reported that platelet parameters were not associated with PDA were also published. We also wanted to contribute to clarify the relationship between PDA and platelet parameters.

Materials and Methods: Preterm infants that less than 34 gestational weeks were examined to echocardiography at the time of detected clinical findings or within 24-72 h after admission to our unit, routinely. The patients were divided into two groups according to echocardiography findings randomly; hsPDA require ductal closure treatment and non-hsPDA. The platelet count, MPV, PDW, PCT and Platelet Mass Index values of both groups were compared.

Results: There was no difference between the two groups in terms of MPV, Platelet count and Platelet mass index. However, PDW and PCT were statistically significantly in the study group than the control group.

Discussion: As a result, according to our study, platelet count, MPV and platelet mass index cannot be used to predict either hsPDA or treatment success, but a low PCT and high PDW can be used predict hsPDA but not treatment success.

Introduction

Patent Ductus Arteriosus (PDA) can cause mortality and morbidity such as respiratory distress syndrome (RDS), pulmonary hemorrhage, bronchopulmonary dysplasia (BPD), intraventricular hemorrhage (IVH), necrotizing enterocolitis (NEC), retinopathy of prematurity (ROP) [1]. For this reason, early diagnosis and treatment of PDA is the most important point. The main diagnostic method of PDA is Doppler echocardiography [2]. However, there is no clearly consensus on diagnosis of hemodynamically significant patent ductus arteriosus (hsPDA). Therefore, new diagnostic methods of PDA are needed. A great number of the studies have shown that platelets play a role in closure of the PDA [3-6]. The first of these studies, Echtler et al. studied the relationship between ductal closure and platelet parameters in animals [3]. In the same study, the ductus arteriosus did not close (thus, remained permanently open) in animals in which platelet functions were compromised. After this study, they studied on premature infants about relationship between ductal closure and platelet parameters. According to this study, a low platelet count and a low PDW were risk factors for PDA. However, studies that reported that platelet parameters were not associated with PDA were also published [7-11]. We also wanted to contribute to clarify the relationship between PDA and platelet parameters.

Materials and Methods

This observational, retrospective cohort study was conducted between August 2017 and 2018. Preterm infants that less than 34 gestational weeks were examined to echocardiography at the time of detected clinical findings or within 24-72 h after admission to our unit, routinely [12]. The patients were divided into two groups according to echocardiography findings randomly; hsPDA require ductal closure treatment and non-hsPDA. hsPDA was defined when at least one of the clinical findings associated with PDA was present: a hyperdynamic precordium; a sustained murmur; tachycardia; hypotension; oliguria; an increased pulse pressure; an increase in ventilation pressure and/or oxygen demand; and at least one echocardiographic finding: ductal diameter ≥1.5mm, left atrium/ aortic root ratio ≥1.5, and/or diastolic flow failure in the abdominal aorta or inverse flow. We applied intravenous or oral ibuprofen to close the hsPDA. Intravenous or oral paracetamol was given in cases who ibuprofen is unsuccessful or contraindicated. After treatment, echocardiography was performed again, and the PDA was classified as open or closed. We excluded those with conditions that might cause inflammation or affect platelet count and/or function (Antenatal steroid use, PPROM, early sepsis, chorioamnionitis, congenital viral infections, preeclampsia), congenital heart disease, pulmonary hypertension, perinatal asphyxia, congenital anomaly, chromosomal anomaly, thrombocytopenia (<50.000/mm3), and lack of data. Written informed consent was obtained from all parents. All echocardiographic examinations were performed by Vivid S6 Echocardiography System fitted with a 10S transducer (General Electric Healthcare, Milwaukee, WI, USA). Blood samples taken from an umbilical venous catheter at between 48-72 hours and 7. day, were collected in ethylenediaminetetraacetic acid-containing tubes and blood counts performed using a Coulter Counter model LH (Coulter Electronics, Hialeah, FL, USA). This yielded the platelet count, MPV, PDW, PCT. The platelet mass index was obtained from the platelet count (10³/mm³) and the MPV (fL). We recorded gestational age, birth weight, sex, mode of delivery, Apgar scores (at 1 and 5 min) 48-72 h and 7. day platelet parameters, surfactant requirement, ventilation history, IVH, NEC, ROP, BPD, duration of hospitalization and any death.

Statistical Analysis

Statistical analyses were performed using SPSS for Windows ver. 22.0 (SPSS Inc., Chicago, Illinois). The paired samples t-test and independent samples t-test were used to compare continuous variables. Continuous variables are presented as means ± SDs, and categorical variables are given as frequencies with percentages. A p-value less than 0.05 was considered statistically significant.

Results

258 newborns under 34 weeks were admitted to our unit, of whom 121 were excluded. The study group consisted of 72 premature infants with hsDPA who applied ductus closure treatment and 65 premature infants without hs DPA or spontaneously closed PDA consisted of the control group (Figure 1). The demographic characteristics of both groups are shown in Table 1. The mean gestational age and the mean birth weight of the study and control groups were, respectively, 31.4±3.8 vs. 32.3±4.5 weeks (p=0.12); 1441±347 vs. 1,539±286g (p=0.08). There was no difference between two groups in perinatal parameters. The platelet parameters of both groups are shown in Table 2. There was no difference between the two groups in terms of MPV, Platelet count and Platelet mass index. However, PDW and PCT were statistically significantly in the study group than the control group.

Table 1: Comparison perinatal characteristics of the study and control groups.

hsPDA: hemodynamically significant patent ductus arteriosus.

Table 2: Comparison of the platelet parameters of the study and control groups.

PDW: platelet distribution width; PCT: platocrit; MPV: mean platelet volume; Platelet mass index: the platelet count (10³/mm³) X MPV (fL); hsPDA: hemodynamically significant patent ductus arteriosus.

Figure 1: Flowchart of study.

PPROM: Preterm premature rupture of the membranes; hsPDA: hemodynamically significant patent ductus arteriosus.

Discussion

Low oxygen pressure, elevated prostaglandin and nitric oxide levels are the main factors affecting continuity of the ductus arteriosus in the uterus. After birth, increased oxygen levels and decreased prostaglandin levels enable functional closure of the DA [13]. In addition to this mechanism, different mechanisms of closure of the ductus began to be discussed. The discussion began when Echtler et al. showed that platelets were attached to the lumen of the closed ductus arteriosus and confirmed this experimental finding via a retrospective study of preterm births [3]. After this animal study, various hypotheses about the role played by platelets in duct closure in newborns have been proposed. The most acceptable hypothesis is an effect of platelets on DA contraction, which occurs immediately after birth in term newborns, triggering hypoxia in the vessel wall by decreasing the blood flow in the venous lumen and vasa vasorum; in preterm newborns, the cells in the ductus wall are fed by the ductal lumen because of the absence of a vasa vasorum. As the ductus wall is thin, contraction is inadequate and endothelial damage and platelet aggregation thus develop because of vesselwall hypoxia. Based on this hypothesis, it was claimed that platelet counts were important in terms of DA closure in preterm infants, as they are in the pathophysiology of adult vascular diseases [14,15]. However, this hypothesis is not supported by the fact that platelet transfusion does not reduce the incidence of PDA in preterm newborns with immune thrombocytopenia and does not increase the PDA frequency in term newborns with severe thrombocytopenia secondary to Wiskott-Aldrich syndrome [16-20].

In Fujioka et al. [21-23]. the platelet count was not related to PDA diagnosis or treatment success. On the other hand, Echtler et al. [3,5,6] reported that a low platelet count increased the hsPDA incidence [24-25]. In some works performed after these contradictory studies, it was reported that large platelets create a greater potential risk of prothrombotic reactions; large platelets are more aggregated than small and normal platelets given the greater number of receptors such as thromboxane A2-B2 and glycoproteins IIb-IIIa on the surfaces of large platelets. It was suggested that the increased metabolic and enzymatic activities of dysfunctional thrombocytes, rather than the platelet count, were associated with PDA [26-29]. We sought to identify parameters related to platelet function associated with PDA. These remain controversial; all of MPV, PDW, PCT, and platelet mass index have been associated with cardiovascular diseases in adults [30-35]. In addition, in a limited number of studies on neonates, the MPV and PDW were shown to be associated with prematurity complications such as RDS and BPD [36-37].

In our study, no difference was found between the platelet counts of the hsPDA and control groups at 48-72 h and 7. day. In addition, there was no difference between the platelet counts of newborn who did and did not fail treatment. In conclusion, the platelet count was not a predictor of hsPDA diagnosis or treatment success. The results of our study contradict those of the two major meta-analyses conducted by Simon et al. and Mitra et al. but support the cohort study of Sallmon et al. [18-20]. PCT was lower and PDW was higher in the study groups than control groups and the difference between the two groups was statistically significant. However, MPV and platelet mass index were similar in both groups. Thus, we conclude that the PCT and PDW can be used to predict hsPDA but not treatment success. Demirel and Dizdar et al. [4]. reported that the PDW was higher in preterm infants with hsPDA than in control groups [38,39]. Bekmez et al [40]. reported that a low PCT increased the hsPDA incidence Demir et al.[41]. found a high MPV and a low platelet mass in the hsPDA group. We also excluded patients who received ibuprofen as ductus closure therapy because of potential effects on platelet count and functions. Infants born to mothers with prior pre-eclampsia, which affects platelet count and ductal flow because of the increased placental resistance, were also excluded [42-44]. We also excluded infants with perinatal asphyxia associated with an increased PDA, thrombocytopenia, and platelet dysfunction [45-47]. Newborns whose mothers had earlier received steroids were excluded because of possible effects on the platelet count. We thus excluded all pathologies that may affect platelet count and function and induce inflammation. There were some limitations of our study. The first limitation of our study is that it was retrospective in nature. The second limitation is modest sample size. As a result, according to our study, platelet count, MPV and platelet mass index cannot be used to predict either hsPDA or treatment success, but a low PCT and high PDW can be used predict hsPDA but not treatment success.

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Lupine Publishers | Msct In Diagnosis of Congenital Heart Diseases in Viet Nam

Lupine Publishers | Advancements in Cardiology Research & Reports

Abstract

Background: Congenital heart diseases associated with more malformations, complex aortopulmonary collaterals and anomalous coronary artery. Echocardiography is the initial diagnostic method but this method can be limited in complex congenital heart diseases.

Purpose: To assess the role of MDCT in congenital heart diseases (CHD) diagnosis compare with operative result and interventional angiography.

Methods: 910 patients with congenital heart diseases of 31.000 patients underwent cardiac angiography with 64 and 320 section CT at Medic Medical Center since 09/09/2006 to 30/12/2015.

Results: There are 658 operated cases, most of operated cases demonstrated the exact diagnosis of MDCT in congenital heart diseases.

Conclusions: MDCT is the fast and non-invasive diagnostic method with the high accuracy, overcomes the limit of echocardiography in complex congenital heart diseases diagnosis and provides the panorama and useful information’s prior to the operation.

Keywords: Congenital heart diseases; Cardiac multi-detector computed tomography, Multi-detector computed tomography in congenital heart diseases; Congenital heart diseases computed tomography

Introduction

Congenital heart diseases effect ~ 1% of all live births in the general population. Complex congenital heart diseases associated with more malformations, complex aortopulmonary collaterals and anomalous coronary artery. Over the past few decades, the diagnosis and treatment of congenital heart diseases have greatly improved [1-6]. Diagnostic tools: X-ray, ECG, echocardiography, MRI and MDCT. ECG and X-Ray suggest the diagnosis but are not specific. Echocardiography is the initial diagnostic method for patients with suspected CHD but this method can be limited in complex CHD. The great capabilities of MRI for anatomic and functional assessment of the heart but MRI is time-consuming and may require patient sedation. Now enable CT to be used as an accurate noninvasive clinical instrument that is fast replacing invasive cine-angiography in the evaluation of CHD [1,2,5].

I. Improves both spatial and temporal resolution.

II. Increases scanning speed.

III. Improves diagnostic image quality by reducing respiratory artifacts

Purpose

To assess the role of MDCT in congenital heart diseases (CHD) diagnosis compare with operative result and interventional angiography.

Material and Methods

Subject: 910 patients with congenital heart diseases of 31.000 patients underwent cardiac angiography with 64 and 640 section CT at Medic Medical Center since 09/09/2006 to 30/12/2015.

Means and scanning techniques

a) Medic Medical Center scanned cardiac CT by 64 MDCT Toshiba Aquilion machine and Toshiba Aquilion One (320 MDCT), 0.5mm slice thickness, 0.5mm imaging reconstruction.

b) Two phases scanning: Don’t inject phase and contrast media injection phase: +Phase doesn’t inject contrast which help locate and assess coronary artery calcification.

c) +Phase inject contrast media: Medicine chasing phase and water chasing phase.

d) Contrast pumping machine is double-barreled Stellant (Medrad).

e) To inject contrast by intravenous right hand.

f) Contrast dose used 1mL/ kg.

g) Drug pump speed depends on patient status and disease.

h) Vitrea software: Reconstructed images by MPR, MIP and VRT.

i) Effective radiation dose is low (320-MDCT is 3.69±061mSv; 64-MDCT is 12-14mSv) (Figures 1).

Figure 1.

Data analysis

a. The prospective study and case series report compare with operative and interventional angiography.

b. Data collection at the HCM city Heart Institute, Tam Duc Heart Hospital and Medic medical center (Figures 2-17).

Figure 2: Atrial septal defects and Ventricular septal defects.

Figure 3: Patent ductus arteriosus.

Figure 4: Coarctation of aorta.

Figure 5: Double aortic arch.

Figure 6: Tetralogy of Fallot.

Figure 7: Pulmonary atresia with ventricular septal defect.

Figure 8: Transposition of great vessels.

Figure 9: Double outlet right ventricle.

Figure 10: Single ventricle.

Figure 11: Aortopulmonary window:

Figure 12: Truncus arteriosus.

Figure 13: Anomalous systemic venous return.

Figure 14: Anomalous pulmonary venous connection.

Figure 15: Single pulmonary artery.

Figure 16: Pulmonary artery trunk aneurysm:

Figure 17: Congenital pulmonary arteriovenous malformation.

Results

There are 658 operated cases, most of operated cases demonstrated the exact diagnosis of MDCT in congenital heart diseases.

Discussion

Congenital heart diseases associated with more malformations, complex aortopulmonary collaterals and anomalous coronary artery. Echocardiography is the initial evaluative method for preand post-operation congenital heart diseases but this method can be limited in complex cases. Multi-detector computed tomography overcomes the limit of Echocardiography by multiplanar reconstruction (MPR) and volume rendered techniques (VRT) reconstruction . Volume rendered techniques (VRT) reconstruction clearly demonstrates the relationship between the heart and great vessels.

Conclusion

Multi-detector computed tomography is the fast and noninvasive diagnostic method with the high accuracy. Overcomes the limit of Echocardiography in complex congenital heart diseases. Provides the panorama and useful information’s prior to the surgery.

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Lupine Publishers | Peer Review of Statistics in Surgical Research: Identify The X-Factor or Toss a Coin!

Opinion

Professor Peter Bacchetti’s excellent article [1], highlighting “the other problem of peer review of finding flaws that are not really there based on unfounded statistical criticism, and its demoralizing effect on authors”. I wish to add some thoughts to the debated issues. Professor David Horrobin’s original classics on the subject [2,3]. have not yet been surpassed. It was updated recently [4] and prompted some contributory thoughts [5]. Having enough experience as author of reject articles and some as peer reviewer, I find the most devastating effect to author’s morale is making no comment, giving no reason for rejection or not replying all. The BMJ is guilty on this account as an article of mine was rejected that was accepted elsewhere after minor editing [6]. The BMJ, however, is in the good company of most biomedical journals who apply the COPE rules. The article lacked statistics of any kind that perhaps might be one of the reasons it was disliked at BMJ. To Editors’ credit, however, it took about a month to say ‘No’ that caused no momentum loss, unlike other Journals who reach the same verdict on other articles after 6 months or a year that drag another year or two before the author could recover and gather enough time, interest and energy to face the damn thing again. One subtle aim of that article [6], mentioned to BMJ Editors, was an attempt to say that “there is science and in particular evidence based medicine without statistics”.

It is a devil’s advocate to say statistics has not only been made into a “big lie” but also ‘false God’. It was invented elsewhere but currently worshiped only at most medical and surgical journals. A look at Science and Nature testifies such prestigious magazines have reduced statistics to real size and value as a “tool for testing a hypothesis”. It is not too basic a question for every biomedical peer reviewer to find out the exact role, aim and limitations of statistics. Some was mentioned in an article [7], nobody noticed save the late great Professor GD Chisholm editor of Br J Urology. It was based on a study that was rejected by a grant committee. It aimed at resolving 2 of the most serious puzzles of current clinical practice, postoperative hyponatraemia and the multiple vital organ dysfunction or failure syndrome [8]. However, giving data and statistics [7,8]. before clarifying the theories [9]. has proved as wrong as putting the cart in front of the horse. Einstein’s methods on proposing the special and general relativity theory is the correct way. When statistics was haled in the sixties everyone thought it was the only mean to discover “The Unifying Theory”.

This has proved both immensely costly and wrong. The basic fact is ‘statistics cannot, was not intended to and will never could, make a discovery’. Observation, mental experiments and the X factor are the only way to make a discovery long before it is verified and proved by practical studies and statistical tests. Before explaining the X-factor please allow me tell a relevant true story that symbolizes the current problem with statistics. Two friends of mine in UK had a disagreement, made a bit on a round of drinks and decided the first person to enter the hospital club will be the judge. Guess who did? I did but having no clue on how to resolve the conflict suggested that a flip of a coin might be the best way. They agreed also to my condition that while head or tail will determine the winner among them, if the coin stood on edge the judge should be the winner of all. It did and I won. Another conflict started on: Who should buy the 3rd round of drinks? Both agreed that it was my turn. I explained that buying the 3rd round will gain good company but lose all winnings, and my turn should be the 5th round! The point is statistics can tell the probability of head or tail and exclude the odd but when evaluating to either 0 or 100% and the truth is known, instead of expiring it generates residual arguments. Professor Richard Smith contributed to this debate by quoting Dr Hedge on Professor Robert Fox’s famous thought that “swabbing the rejects with the accepts does not make a difference.”

He added that perhaps it has already been done at BMJ” and asked “How can you know?” With due respect Sir, I frankly think nobody can. Despite a proven incremental value of an average article it does not make a noticeable difference or great loss to scientific advances. Statistically speaking that means a quality article submitted to BMJ has 50% chance of being accepted or rejected. So, why not save everybody the trouble and toss a coin? Here is where statistics has shot itself in the foot. It gives an average chance to the average and an odd chance to the odd but can’t tell which is important. The odd chance of a tossed coin to stand on edge matches that of a breakthrough scientific or medical article coming an editor or peer reviewer’s way but detecting such article makes all the difference. Some call it a hunch or gut feeling. Others qualify it by the three-pronged tests of quality, relevance and civility. Identifying the “X-factor” that makes such an article stand out is worth all the trouble. I honestly do not know but it is the arresting beauty found in Einstein’s famous papers, Newton’s laws, Mozart’s music and Shakespeare’s writing among many examples that include medicine [2-4]. I wrote 2 articles on such para-scientific para-medical stuff to identify the X-factor, “Rules and lures of the science game” and “The Mozarts of Science” sent to journals nearly two years ago and have not received a reply yet. I think a message of “Ignore the big headed bustard” arrived. Qualified people to find out the X-factor are COPE members. Another question that requires a ‘Yes’ or ‘No’ answer would be: if any of Einstein’s papers is evaluated using the current peer review standard and statistics adopted by most biomedical journals, would it be accepted?

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Lupine Publishers | Non-Compacted Cardiomyopathy: Is there a Need of a New Cardiomyopathy?

Lupine Publishers | Journal of Cardiology & Clinical Research

 

Abstract

Left ventricular non-compaction (LVNC) is a myocardial disorder, classically defined as a double-layered myocardium, consisting of a thick, spongy/hypertrabeculated, non-compacted endocardial segment and a thin, compacted, epicardial portion. The American Heart Association (AHA) classifies LVNC as a distinct primary genetic cardiomyopathy, while the European Association of Cardiology (ESC) as an unclassified cardiomyopathy. Despite the magnitude of the entire literature yield on this topic, to date the pathogenesis, prognosis, and treatment are still unclear. Prevalence and mortality can range respectively from 0.05% to 0.26% and 5% to 47%, but they are affected by the imaging criteria adopted for the diagnosis. In fact, LVNC has been for years incidentally discovered during autopsy of unexplained sudden cardiac deaths. Conversely, with the advent of increasingly sophisticated cardiac imaging techniques, the presence of hypertrabeculated myocardium has become very common. Both echocardiographic and magnetic resonance criteria have been proven to overestimate the diagnosis, which shares a peculiar phenotype with other pathologies. It is known that a hypertrabeculated left ventricle leads to a symptomatic triad consisting of heart failure, arrhythmias and thromboembolisms. Therefore, it is current opinion of the authors that a “non-compaction cardiomyopathy” (NC-CMP) seems to be the most comprehensive definition of a disease that, similarly to the other cardiomyopathies, and regardless of its etiology, beyond a peculiar phenotype shares a distinct symptomatology and deserves to be listed as an entity between cardiomyopathies.

Keywords: Left Ventricle Non-Compaction; Non-Compacted Cardiomyopathy; Cardiomyopathies; Heart Failure; Sudden Cardiac Death

Introduction

Left ventricular non-compaction (LVNC) is a myocardial disorder, classically defined as a double-layered myocardium, consisting of a thick and spongy or hypertrabeculated endocardial segment, defined as non-compacted, and a thin and compacted portion, laying epicardially [1]. The above-mentioned hyper trabeculations (HXTs) characteristically involve the left ventricle (LV), especially the apex, the lateral, infero-lateral and inferior wall [1,2], and less frequently the right ventricle [3]. Since its first reports, LVNC has always been considered a controversial pathology (Figures 1 & 2). In facts Grant and colleagues, for long accredited as discoverers in 1926, presented a case of persistent sinusoids instead of LVNC [1]. In addition, a lack of uniqueness among the World Health Organization [4], the European Society of Cardiology [5]. and the American Heart Association [6] for its classification, and the presence of trabeculae as a terminal phenotype of LV hemodynamic overload or other myocardial affections, has led several authors to debate on the real existence of a true form of uncomplicated primitive non-compacted cardiomyopathy [7,8].

Figure 1: Two different anatomo-pathological macroscopic sections of the left ventricle, presenting a non-compacted myocardium. Modified from Lorca et al. Int J Cardiol 2016.

Figure 2: Echocardiographic features of a young adult of 16-years old, admitted in emergency room with acute signs and symptoms of acute heart failure.

Morpho Pathogenesis

The primitive hypothesis concerning LVNC is that the presence of HTXs is due to a failure in myocardial morphogenesis, in which the immature, non-compacted fetal myocardium normally undergoes a physiological compaction process during ontogenesis [1]. LVNC may occur isolated, in familial forms or associated with several congenital, genetic, neuromuscular and chromosomal conditions [9]. Mutations in the sarcomere gene, particular in MYH7, are the most common and non- sarcomere gene mutations (such as TAZ and NOTCH1) have also reported [10-12]. Some LVNC individuals have been detected by tracking asymptomatic relatives of affected patients [9], and therefore, a close correlation between genotype and phenotype has been recently underlined by 2 recent studies using NEXT-generation sequencing [13,14]. All these pathogenic variants were independent risk factors for cardiovascular events [13]. In addition, mutations in hyperpolarization-activated cyclic nucleotide channel 4 (HCN4) have also been reported in families with sinus node dysfunction and LVNC [15,16].

Epidemiology

Since only few studies focused on LVNC incidence, both prevalence and mortality are challenging to assess [1]. Among adults, it can be diagnosed in 0.05% - 0.26% of the cases, and approximately 0.14% of pediatric patient, with an overall mortality ranging from 5% to 47% in both populations [1]. Unfortunately, all the reports are affected by the diagnostic criteria adopted, imaging or autopsies, overestimating or underestimating the real prevalence [1,17] .In addition, and similarly with others cardiomyopathies, LVNC can be a subtle disease [17]; if not promptly diagnosed, patients may be asymptomatic for a long time and the onset may range from the early life to the adulthood [8].

Diagnosis

The advent of increasingly sophisticated cardiac imaging techniques set the spotlight on HXTs as a very common finding, instead of the rare disease that was previously considered [2,18,19]. Accordingly, Jenni, Chin and Stollberg defined different echocardiographic criteria, while Petersen, Jacquier, Captur and Stacey defined some cardiovascular magnetic resonance (CMR) criteria. 1 Unfortunately, they both showed very poor specificity [7,8], even if CMR overcame the ultrasound-related limits in morphologic assessment, and demonstrated a thigh correlation between late gadolinium enhancement myocardial fibrosis and clinical severity of the disease [20]. Nevertheless, there still a lack of an imaging-driven diagnostic gold standard [1,9].

Clinical Aspects and Treatment

Clinical findings are variable, including several grades of diastolic and systolic dysfunction, heart failure (HF), thromboembolic events, and malignant arrhythmias. 1 However, the most severe outcome is the sudden cardiac death. Atrial fibrillation, right/left bundle branch block, and repolarization abnormalities may be the only electrocardiographic features present at the moment of the diagnosis [2,8]. There is no specific therapy and LVNC management depends on the clinical manifestations; anticoagulation is indicated only if atrial fibrillation, heart failure, previous embolism, or intracardiac thrombus formation are present [1,21].

Discussion

LVNC has always been a controversial disease, with some unresolved issues. First of all, there is a heterogeneous genetic background and a wide spectrum of associated conditions that may occur contextually with HTXs. Secondly, LVNC real prevalence is still unknown. Certainly, the lack of any echocardiographic or CMR diagnostic gold standard, with frequent overestimation/ underestimation, does not help to clarify all the uncertainties. In addition, there are a wide variety of overlapping conditions that may occur with secondary myocardial HXTs, for example, a dilated cardiomyopathy or the end-stage hypertrophic cardiomyopathy (Figure 3). On the other hand, it is common experience that not all the above-mentioned cardiomyopathies and conditions can present an end-stage non-compacted phenotype and generalizing this aspect would be very simplistic. 8 In addition, Lorca and colleagues recently reiterated that non-compacted forms of cardiomyopathy do exist, especially during early stages of life, and they can be demonstrated in some forms of unexplained sudden deaths. 17 Furthermore, a multicenter longitudinal prospective study [7], despite its conclusions, and if carefully read between the lines, suggests that a significant proportion of asymptomatic patients meets all currently used imaging diagnostic criteria for LVNC.

Figure 3: Cardiac magnetic resonance imaging (CMR) exams of patients matching the currently imaging criteria for CMR (A, B, C, 2-chambers view; a, b, c, 4chambers view). (A, a) A 23-years-old male patients with a dilated cardiomyopathy. (B, b) a 38-years old woman with an end-stage hypertrophic cardiomyopathy. (C, c) a 45-years old woman admitted in emergency room for acute heart failure, and history of silent cerebral infarcts.

However, they demonstrated that outcomes are increased by symptoms and clinical conditions when associated with a noncompacted phenotype. Indeed, a recently published multicenter register provided an accurate estimation of genetic-phenotype association, and clinical and events of LVNC patients, concluding that the clinical course of symptomatic LVNC patient with a genotype-phenotype matching can be severe [13,14]. Given all these premises, it is reasonable considering the existence of a primitive non-compacted disease, congenital, and a mild form, with a late-onset, and/or acquired conditions. HF, thromboembolic events, and malignant arrhythmias seem to constitute the clinical triad for LVNC patients, and sudden cardiac death the most severe outcome. There is a tight genotype-phenotype correlation, with a wide spectrum of genes and mutation involved, as well as hypertrophic cardiomyopathy, for example, and the current imaging-derived diagnostic criteria probably need to be revised; perhaps it should be worth to combine some imaging and clinical criteria. At last, multicentric registries should be considered to help the real prevalence assessment of non-compacted forms of cardiomyopathies.

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Lupine Publishers | Troubleshooting in Upgrading Procedure: Intraprocedural Percutaneous Transluminal Angioplasty of Great Vessels

Lupine Publishers | Journal of Cardiology & Clinical Research

 

Abstract

Upgrading procedure is relatively common since indications to cardiac resynchronization therapy (CRT) and implantable defibrillator are increasing. A relatively frequent phenomenon that the operator may encounter is some degree of venous obstruction around the previously implanted leads, which may become completely occlusive. In these situations, upgrading procedure may be challenging and various manoeuvers have been described. We describe a case of intraprocedural percutaneous transluminal angioplasty (PTA) of occlusive stenosis of the innominate vein, performed during an upgrading procedure from bicameral cardiac implantable defibrillator (ICD) to CRT-D.
Keywords: Upgrading; Cardiac resynchronization therapy; Percutaneous transluminal angioplasty; Venous occlusion

Introduction

Cardiac resynchronization therapy is a well-established therapy for patients with severe systolic dysfunction, wide QRS and heart failure despite optimal medical therapy [1]. Moreover, since indications for cardiac resynchronization devices continue to expand, the number of upgrading procedures from previously implanted single- or dual-chamber systems is increasing. In these cases, some degree of venous obstruction is a relatively frequent phenomenon (up to 50%), which may become completely occlusive in 12% of cases [2]. Chronic venous occlusion, mostly asymptomatic, can involve the coronary sinus and its branches as well as central veins, such as the axillary-subclavian or innominate veins. Angioplasty of the coronary sinus is well described in the literature to allow the placement of a left ventricular lead (LV) [3,4]. By contrast, not many data are available on the intra-procedural safety and efficacy of central vessel angioplasty [5,6]. We describe a successful case of angioplasty of a total central venous occlusion to allow LV lead placement during an upgrading procedure to a CRT system.

Case Report

A 69-year-old patient with a clinical history of hypertension, diabetes, prior myocardial infarction, poor EF (30%), and previous percutaneous transluminal coronary angioplasty (PTCA) on the circumflex coronary artery, was referred to our institution for elective replacement of a dual-chamber ICD implanted in July 2008 (ICD Lumos DRT, atrial lead Selox JT 53 and ventricular lead Linox SD 65/16, Biotronik SE. Berlin Germany). On admission, the patient was symptomatic for dyspnea, with a poor functional class (NYHA III), the echocardiogram showed a severely depressed ejection fraction (20%) and the electrocardiogram confirmed a wide QRS duration of 130msec with left bundle branch block. A coronary angiography confirmed the indication to medical therapy in the absence of any target vessel for revascularization. We consequently decided to perform an upgrading procedure to a CRT system. In accordance with our clinical practice, angiography of the axillary and subclavian veins through the ante cubital venous access was performed before the procedure to assess patency of the central veins. The angiogram documented severe stenosis of the axillary vein at the insertion point of the right atrial and ventricular leads into the vessel. The subclavian vein was then directly punctured distally to the sub-occlusive stenosis (behind first rib), to obtain a venous access for the LV lead. Unfortunately, subsequent advancing on the 0.035” guidewire through a sealed 9 Fr introduction sheath (Safe Sheath HLS 1009, Pressure Product, San Pedro, USA) proved unsuccessful owing to another occlusion at the junction between the superior vena cava (SVC) and the innominate vein, where the second shocking coil lead was located. Selective injection of contrast media into the subclavian vein through the introducer confirmed total occlusion of the main vessel and a wide collateral vicarious circulation draining blood into the SVC (Figure 1).

Figure 1: Vein angioplasty procedure. A. Angiography from the subclavian venous access, revealing occlusive venous stenosis of the anonimous trunk. B. Balloon inflated up to 8-10 atm. across the stenosis. C. Restoration of venous patency after angioplasty.

A 0.014” angioplasty guidewire (TERUMO Corporation, Tokyo, Japan) was threaded through the occlusion and then left in the right atrium. An angioplasty balloon (Sterling 6mm x 20mm, Boston Scientific Inc. Natick, USA) was then advanced over the wire to the occlusion and inflated to 6 atm. In order to progressively open the occlusion, we removed the balloon and advanced over the 0.014” wire a multipurpose catheter (Cordis Corporation, Miami, USA) which, thanks to the dotter effect, enabled us to pass through the stenotic tract and to replace the 0.014” with a 0.35” x 200 cm guidewire. Once we had retrieved the MP catheter, a larger angioplasty balloon (Sterling 8 mm x 40 mm, Boston scientific Inc. Natick, USA) was advanced over the 0.35” wire and repeatedly inflated to 10 atm to obtain satisfactory dilation of the subclavian and innominate veins (Figure 1B). A 5-10 cc injection of contrast medium confirmed the re-establishment of flow within the subclavian vein and SVC, with a residual stenosis of 30-40% (Figure 1C). Implantation of the CRT device was then successfully carried out, without complications, by cannulating the coronary sinus through a dedicated delivery system (Attain Command Straight, Medtronic Inc. Minneapolis, USA), placing a 4 Fr dual-unipolar LV lead (Attain Ability 4196- 88 cm, Medtronic Inc. Minneapolis, USA) into a lateral coronary vein and, finally, by connecting the three leads to a CRT-D device (Consulta CRT-D, Medtronic Inc. Minneapolis, USA). The acute LV lead threshold was 1.1 V at 0.5 msec, with no diaphragmatic capture at 10V. The electrical parameters of the right atrial and right ventricular leads were also stable. The additional time required to perform PTA was 15 minutes, plus 3 minutes of fluoroscopy time with an additional 30 cc injection of contrast medium injection. At the 3-month follow-up examination, electrical parameters of atrial, right ventricle and left ventricle leads were stable, and no adverse event was observed.

Discussion

Chronic venous occlusion is not an infrequent finding in patients undergoing implantation procedures. This issue may involve both the coronary sinus and the central venous system. Recognized risk factors for venous obstruction include blood stasis due to venous angulation or kinking, the presence of a central venous line for long-term infusion therapy, hemodialysis, trauma, infection and the presence of pacemaker leads. Heart failure and poor systolic function may facilitate the process [7,8]. The most likely pathogenesis seems to be due to thrombosis, beginning with fibrin deposition over the lead surface and progressive fibrous reaction, with a ring-like fibrosis development around the lead, causing severe stenosis or even total occlusion of the vein [5]. The presence of a second ICD shocking coil, usually located in the superior vena cava, has been associated with increased incidence of venous obstruction [9]. In our case, the occlusion was localized at the junction of the innominate vein with the superior vena cava, where the second shocking coil lead lays for anatomical reasons. Thrombosis and fibrotic reaction were probably favored by the close contact of the heavy coil with the vessel wall at a point where, for hemodynamic reasons, there may be turbulence, thereby predisposing the vessel to occlusive stenosis.
As the stenotic process is usually gradual, a collateral venous network can develop to compensate for the occlusion. Consequently, symptoms or physical signs are rare, and partial or total venous occlusion may be totally asymptomatically, becoming an unexpected finding at the time of implantation. If a new lead needs to be added to the implanted system, the operative strategy may differ considerably according to the physician’s familiarity with the available technical options. The physician can choose among various approaches: an opposite-side approach with subsequent lead tunneling across the thorax [10], an ipsilateral approach performed by means of jugular system cannulation [11], and epicardial placement of the leads through thoracotomy or vein angioplasty [5]. The first option carries several risks, including the development of complete occlusion of both subclavian veins over time, damage to the leads — particularly deleterious in the case of ICD leads - or higher defibrillation threshold in the case of rightside placement of the active can. The jugular system approach may expose the patient to the risk of worsened blood drainage or, in the case of the internal jugular cannulation, even acute serious damage to this important vessel of the neck [12]. Epicardial placement of the leads through thoracotomy has the disadvantage of requiring surgery and general anesthesia.
Our experience showed that angioplasty of the central venous system can be performed in the same session of the upgrading procedure without excessively prolonging the procedural time, thereby avoiding postponing the procedure. We observed no complications, damage or dislocations of the existing leads. Moreover, this approach is less invasive than other alternatives and allows the patency of the contralateral venous system to be preserved. This case also shows that in certain clinical conditions at higher risk of venous occlusion, it is advisable to perform an angiography from ante cubital vein before the procedure, in order to assess the patency and exact location of the great veins. We can hypothesize that incomplete location of the second shocking coil inside the superior vena cava and the lying of the coil across the junction between the innominate vein and superior vena cava may contribute, for hemodynamic reasons, to the development of a marked fibrotic reaction. Eventually, in case of occlusive stenosis of central veins, intraprocedural venoplasty of great vessel seem to be feasible, without postponing the upgrading procedure.

https://lupinepublishers.com/cardiology-journal/pdf/ACR.MS.ID.000128.pdf  
https://lupinepublishers.com/cardiology-journal/abstracts/troubleshooting-in-upgrading-procedure-intraprocedural-percutaneous-transluminal-angioplasty-of-great-vessels.ID.000128.php

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