Questions related to Clinical Cardiology
At what AAA size would you consider Cardiac Nuclear PET/SPECT with Lexiscan over Dobutamine Stress Echo? (outpatient setting)
How important is the potential for a hypertensive blood pressure response with use of Dobutamine?
How important is the presence or absence of a previously placed graft?
What are other clinical factors on which you would base your decision?
-comments greatly appreciated!
Deborah Williams, NP
Plaques form due to a self-healing mechanism of blood vessels and will increase over time. When entering blood vessels, they block blood flow, lead to hypertension and decrease blood flow to organs such as the heart. To get rid of these plaques, we need to boost the good cholesterol such as HDL or improve health of liver to produce enzymes that move these plaques. So, what other ways to get rid of these plaques without using invasive methods?
Thanks and best regards.
I would like to ask your opinions on an interesting case:
46 yr old female patient had an infection of uppper respiratory system in the beginning of September. Shortly afterwards she developed angina pectoris like symptoms. EKG was without pathological signs. In 24h-EKG only a sinus tachycardia showed, when walking slowly (up to 140-160 beats /minute). Echocardiography was without pathological signs as was lab (CRP, troponin, myoglobin, hemoglobin,...). In a cardio-MRI in November a cardiac microvasculatory dysfunction (endothelialitis? small vessel disease?) was diagnosed.
In a blood test, troponin, creatine kinase, creatine kinase-MB, CRP, c-ANCA, p-ANCA, lupus anticoagulant, anti-cardiolipin antibodies... and so on all were negative.
Only antibodies against endothelium could be shown.
Does anybody here have experience with a case like that? At the moment, we think mainly about an autoinflammatory process (e.g. triggered by auto-antibodies). Is there any way to find evidence pro or con?
What shall be the choice: manual or automatic? It is clear from research and practice that inaccuracies exist with automatic BP use while manual seem preferable or yet not really? Some claim that automatic exclude bias in measurement.
Inaccurate reads of blood pressure lead to consumption of medications otherwise not needed if blood pressure measurements would be accurate. It affects lives-health. Which BP monitor shall be used? Both? How to resolve this dilemma in our age of automatisation?
I know that much inquiries are made by me but its a life related investigation.
Thank you in advance for contributions.
I have recently repeatedly observed pulmonary haemorrhage in association to an appropriate use of the LUCAS device by different team for OHCA CPR. This was very different from haemorrhagic secretions, that can somtimes occur during prolonged CPR.
Any thoughts or experience?
Is there any research on if/how a slightly dilatated thoracic aorta root dilatation (caused by high blood pressure and not Marfan) can be successful reversed? If not, what is the physiological reason that a dilatated aortic root (4cm) (caused specifically by high blood) pressure cannot return back to normal size after aggressive blood pressure control?
A 40 days premature neonate reffered other center due to large ra thrombosis.
.he hasn't positive history of cvp catheter .
in examination ,stable hymodynamic , normal saturation , gread 2/6 systolic murmur ,no sign of respiratory distress.
in echo: a large echogenic ,pedinculated ,moveable thrombus protruding to tv ,area about 1.1 cm2 ,mild tr with p.pg= 27 mmhg ,otherwise is normal .
what is your opinion about managment of this neonate?
58 year man with Achalasia cardia who underwent Trans thoracic Heller"s cardio myotomy in 1962, started c/o of regurgitation of liquids from nose and mouth mostly at night for over one year.Details of the procedure are not available.Requested to have Upper GI scopy,Manometry and 24hr PH.Not a diabetic or Hypertensive.No respiratory symptoms.
Is Hypertension only risk factor for Abdominal Aortic aneurysm or it can be a risk factor for Thoracic aneurysm as well ?
The fibrotic response after a myocardial infarction (MI) can be classified into two types of fibrosis:
1-Replacement or reparative fibrosis at the infarcted area (scar formation)
2- Reactive fibrosis outside the infarcted area usually after the replacement fibrosis
The replacement fibrosis or fibrosis healing phase (takes 4 to 6 weeks post MI) is a pivotal process to prevent the rupturing of the ventricular wall after an ischemic insult. However, is it wrong if we disrupt this process?
I would be grateful if you could give me anything about this topic.
This is a left parasternal short axis view at the level of aortic valve and pulmonary artery in a 29 years full term pregnant female, she was asymptomatic, no abnormality detected on auscultation, echo was indicated before CS.
In your opinion, what this flow stands for ?
We want to know the most common polymorphism of β adrenergic receptor gene associated with bisoprolol therapy in heart failure studies. We want replicate in our population.
Can in future combined CT FFR and CT coronary angiography replace invasive coronary angiography for diagnosis of CAD ?
Is there a different CVD risk profile in Senegal? How has the prevalence of rheumatic heart disease and coronary artery disease changed over time?
Generally systolic thrill is absent in severe TOF.. According to standard book teaching.. We are seeing fair number of patients of severe TOF with systolic thrill... They generally have good size pulmonary artery with pure valvular PS.. Anybody can share personal experiences..
It seems that there are other causes of decreased EKG voltage than pericardial effusion according to publications I have found, but what are they?
A long standing hypertensive patient with heart failure of reduced ejection fraction. He is in functional class II and recently presented with bradycardia increasing fatigue.
I have been reading about various drugs inducing anti-remodeling effects in animal models (rats) of myocardial infarction. Can someone suggest why ischemia-reperfusion is not preferred in this regards and permanent ligation of the coronary artery is preferred? Is it because of the influence of reperfusion on infarct size, thus "reperfusion" itself may mask the true effect of therapeutic drug?
Echo helps in seeing the chambers and valves at the same time. It seems to be a better option for diagnosing congenital heart diseases. What benefits of ECG have led to this research?
A mini-case report. History-evolution of the family disease from peripartal CMP to cardiac transplantation:
- Disease manifested in 35-year-old female to the last trimester of the pregnancy as peripartal cardiomyopathy. Heredity is burdened by the SCD of her mother at the 29-year age.
- ECG 2015: a high voltage complex, WPW phenomenon. ECHO: LV EDVol 187 ml; LV ESVol 135 ml; LVEF 28%; GLS -10.4%;
After 12-18 months post delivery the condition worsened. There were signs of progressive heart failure with biventricular dilatation and systolic dysfunction.
- ECHO 2017: LV EDVol 290 ml; LV ESVol 242 ml; LVEF 17%; GLS -5.1%;RV EDVol 64 ml; RV ESVol 43 ml; RVEF 32%; GLS -9.8%; TPSE 12 mm; index of myocardial mass is 135 g / m2, RV free wall thickness 8 mm, LV free wall thickness 9 mm.
- ECG 2017 : Atrial Flutter, atypical LBBB pattern with "pseudo-infarction" signs of Sodi-Polares (QS in I, avL, V5-V6) and Cabrera (V4).
N-terminal proBNP 16766 pg / mmol.
Cardiac MRI revealed signs of subendocardial linear fibrosis (areas of poor gadolinium uptake that indicate scarring).
ECG and MRI results are in the attached file (mother)
A successful heart transplant (HTx) was performed in the patient.
Since our patient has three children - sons 16,10 and 2 years old, we examined them: Еcho normal, ECG abnormal (see the file attached below).
What cardiomyopathy needs to be differentiated in children under dynamic follow-up? What potential genes should be examined?
A 22 years old male patient had achalasia diagnosed 3 years ago by CT chest with oral and iv contrast, barium swallow and manometry He had endoscopic dilatation 4 times with temporary relief followed by lap. Heller cardiomyotomy 2 years ago with improvement of dysphagia for 3 months only. He had open Heller 4 months ago with improvement of dysphagia for 3 months and then he has dysphagia again. Barium swallow repeated 1 week ago showing achalasia.
Here are strips HM ECG from 19-year-old asymptomatic girl. However, the maximum sinus heart rate during daily monitoring was 64 BPM, and 79 BPM when the test with physical exercise was performed (test accompanied by ventricular and supraventricular extrasystoles). Echocardiography revealed mitral valve prolapse (3,5 mm A2 with minimal mitral regurgitation) only.
Is there a need for additional examination and what to do next research step?
Most of the literature refers to increased troponin in serum as a biomarker but I am interested in knowing if decreased levels in the heart indicates disease.
Given the recent JAMA Internal Medicine Wang et al article on the role of dietary fat in cardiovascular disease, what should clinical cardiologists be advising highly motivated patients with high (>1,000) coronary calcium scores about diet? Would this vary depending on patients' other risk factors?
Is uncontrolled blood sugar raise LDL-C? or there are other factors participate in leading to heart disease?
All the best
A 84 year old woman with hypertension, 2 type diabetes mellitus and chronic renal failure (GFR 30-50 ml).
2005 NSTEMI: LAD and LCX PCI
2006 angina pectoris: distal RCA PCI. LAD and LCX stents no changes
2014 UA: RCA ISR. 1 BMS implantation. Other stents without ISR
Echocardiographia all the time showed good systolic ejection fraction with good wall motions.
In 2014 starts: in ECHO showed a non siginificant pericardial effusion. After coronarographia seen hematuria and anemia.
An urological examination was negative for tumor, but an pelvis CT was done, whith some negative result.
2014.07 gastroscopia: duodenitis erosiva and chronic erosive gastritis was.
2015.08.03-04 was admited with melena. Gastroscopy and colonoscopy was not showed a point of bleeding. 3 U of blood was transfused.
An echo showed a significant pericardial effusion and a pericardiocentesis was performed. 1200 cc. straw-yellow liquid evacuated. And other day 100 cc.
2015.08.05-12 admited to hospital with anemia for blood transfusion. Colonoscopy was done again. The source of bleeding was not found. A polyp of the Bauchin valve was cut of.
The histology result of the colonoscopy sample not confirmed malignancy.
2016.01.05 Admited agin with huge pericardial effusion and symptoms of HF. 1500 cc straw-yellow liquid evacuated. A pleural effusion was this time and a diagnostic thoracocentesis was done.
The results from the pleural fluid showed a sigillocellulare cc. cells
The CA 125 was elevetad. (95 the normla range upper limit is 35 at our lab)
Pericardial fluid: eosinophil cells, mesothel and lymphoid cells was seen.
An cardiac MR was done with negative result for a autoimmune disease or primer cardiac malignancy.
An chest CT was done: negative for cc.
An abdominal and pelvis MR was done: at the point of obturator in both side an 6 mm diameter lymphaticus nodus was detected. In the corpus of uterus an 8 mm myoma detected (T2)
The hemoculture results is negative
2016.04.20 was admited with huge pericardial effusion. 1200 cc bloody liquid was evacuated.
And now 2016.05.31. Again was admited with effort dyspnoe and not a very huge pericardial effusion.
The pericardial effusion sizes was 30-35 mm mostly left side and 25 mm from apex and right side.
The gastroentereologist, onkologist, gynecologist and urologyst do not know the reason of chronic pericardial effusion. Please help, what is the diagnostic option which can use to find the cause of pericardial effusion.
Thank you that you read and help.
I would be happy if someone can look on the enclosed paper and help me to understand the meaning of each of the 3 lines in fig. 1 (also the horizontal dotted line). (The general idea of the figure is clear).
Many thanks, Ran
I would like to know your experience about filling out medications and the corresponding doses when you conduct a clinical trial that primarily doesn't aim to examine the effect of drugs. However, the drugs might affect the final results. When I see the publications of different clinical trials (particularly, in cardiology), usually they just mention the substance group (ACE-inhibitors, statins, etc.) without further giving information about the dosage or particular substance names.
Therefore, the question is - whether you just fill out the substance group of current medications that patient takes (e.g. beta blockers, ACE-inhibitors, statins) or you write down, for example, metoprolol, ramipril, atorvastatin? What about dosages - how do you note, for example, the dosage of Ivabradin 5mg that needs to be taken twice a day? Do you write down the cumulative daily cumulative dosis (10 mg) or the dosis that needs to be taken each time (5 mg)?
Thank you very much in advance!!
The image becomes visible after opening the question. The ensuing discussion provides the interesting bottleneck of this problem though. Any help would be much appreciated.
PS. the last sentence on the image is irrelevant and should have been cropped.
There seems to be a lot of websites referring to cardiospasm and achalasia of the oesophagus as an anatomical problem, but little about acute cardiospasm as an emotionally-induced reaction. I remember as a student seeing a man visiting his father in hospital (from an arab country) overcome with grief and doubled-over with intense pain beneath his lower sternum, and this responded to quiet reassurance from the senior physician who reassured me that this was cardiospasm which would clear up within an hour, which it did. Thanks for any insights from others who have seen this.
A recent meta-analysis on clinical use of PEA (https://goo.gl/k6TKwP) has clearly shown good results. Opinion on the efficacy of this product are anyway conflicting. I would very much appreciate if I could directly correspond with clinical users.
When a patient is diagnosed with arrhythmogenic right ventricular cardiomyopathy (ARVD), first-degree relatives should undergo screening for ARVD. What is the best/recommended screening protocol for first-degree relatives? How often serial follow-up evaluation in individuals at risk of developing ARVD (first- degree relatives) should be done? As electrical abnormalities precede detectable structural changes in subjects at risk for ARVD, should screening with serial ECG and Holter be enough or you recommend also periodical imaging diagnostic (echo/CMR). Do you have different screening protocol for relatives with the presence of a pathogenic mutation (mutation carriers) or relatives of a mutation-negative proband.
What is your experience and how often do you use signal-averaged ECG as one of the criteria (Task Force criteria) for diagnosis of ARVD?
Data is conflicting whether the addition of surgical ablation technology achieve the same sinus rhythm restoration as to historic controls of Cox Maze III patients. That might be related to different surgical eras, different types of rhythm assessment during follow-up or the precision to get transmurality lesion set.
Is collapse from commotio cordis immediate or can the subject still walk around for a bit? Would the subject collapse onto their back and still be able to get up while in this devastating cardiac arrythmia?
There are many articles devoted to the assessment of stroke volume (SV) by the method of impedance cardiography (ICG). There is a description and bioimpedance devices that determine the breathing cycle. But we didn't find studies in which these two characteristics were determined simultaneously.
Does anyone use Definity contrast agent as a continuous infusion? We have had to manually continuously rotate the syringe pump during use to keep the solution mixed. Any ideas on a better method of mixing during infusion? Thanks in advance.
Why was left out the therapy of endocarditis on PM electrodes? How you comment it. And how will you treat it?
Thankx for the answers!
Following ST Elevation Myocardial Infarction (STEMI) the myocardial ischemia causes an inflammatory response, which is a predictor of mortality and myocardial remodeling. Treatment with statins have been shown to be able to reduce the area at risk by reducing inflammation in hypercholesterolemic patients with unstable angina. It is unknown whether the anti-inflammatory effect can really reduce the size of myocardial necrosis in STEMI and if this is due to the anti-inflammatory effect of statins. What would be the best way to advance in the anti-inflammatory strategy for treating STEMI?
I am looking for clinical experience or studies that deal with intra-aortic ballon pump patients and physical therapy exercise protocols while still on balloon pump.
41 years old man who had three vessel CABG (LAD-LIMA, RCA-Ao,Cx-Ao) two years ago.
He had history of recurrent exertional angina, poor exercise tolerance despite maximal medical therapy for the last six months. Therefore we performed coronary angiography. Angiography showed patent grafts of LAD-LIMA, RCA-Ao, Cx-Ao. However, the large side branch of LIMA had not been ligated. The side branch can be coronary steal.
What we do ?
I am interesting to find the answer to a question related to using Kubios (in particular it would be good to get advice from Mika Tawvainen who created the software but if anyone knows anything about this software I would very much appreciate your help).
I want to remove artifacts from some collected HRT and HRV data. My other colleagues have suggested that only automatic filters can be applied to parts of the data. However, the User's guide of Kubios seems to suggest you can remove artifacts manually.
If this is so am I correct in understanding that this can only be done using the ECG data but not the RR interval data displayed on the Kubios data browser?
If this is the case as well, is it right to assume that in order to manually remove artifacts you would want to find data points on the RR interval data browser that seem like artifacts (e.g., they spike up very quickly and suddenly) and then find the corresponding part on the ECG data display and add a marker which would remove the data point so that it is not included as an R wave in the RR interval data browser. By doing this all the artifacts that seems like real R waves will be removed from the data resulting in "clean data" as free from artifacts as it is possible to get it.
If this is all correct then I would assume my colleagues were not aware of a manual function to remove artifacts (i.e., they just used the automatic low, medium and high level artifact corrections) because their data did not have the ECG information which I underestand is required to manual remove artifacts.
It would be great if corrections can be made to my understanding where required.
I would like to know the experience they have with the closure of the atrial septal defect in adults by interventional catheterization?
In patients previously operated for pulmonary valve stenosis, it is advisable to close a defect of atrial septation or better leave the default...???
Thank you very much in advance
I am trying to understand what biomarkers I can use to predict fibrosis and recurrence of AF in a given patient population.
Does anyone know if others exist besides ST2, Galectin-3, TGF beta and TNF-alpha?
DM is known to longer the QT intervals and there is evidence that NAFL also longers the QT intervals. what are the other effects and possible mechanisms?
Psychiatric patients usually take many different medications and often they have been already treated with beta-blockers. However, there are several cases in where You should add beta-blockers, because of newly recognized heart failure or even atrial fibrillation. Often psychiatric patients take medications, which included antipsychotics or even worse an antipsychotic polypharmacy or combinations with antidepressants. According to the survival studies We know that treatment with beta-blockers in patients with stable heart failure (EF less than 35 %) is necessary for better surviving.
The third group of cases consists the consequences of psychotropic medications adverse events (e. g. arrhythmias and clozapine or olanzapine) or prolonged QTc and supraventricular arrhythmias (e. g. amisulpride with clozapine combination or ziprasidone use and escitalopram together). In these cases a trial with beta blockers is usually a first step before drug discontinuation.
From EBM we know that combination of clozapine and amisulpride is benefitial in short term trials, however long term use should lead to several complications in this field.
To sum up, DDIs with psychotropics and beta-blockers should be calculated before prescribing beta-blockers. For example, atenolol is not appropriate with several antipsychotics and antidepressants (QTc prolongation). Also story with metoprolol is more or less the same, however metoprolol is very selective for B1 receptors, however there are cases of induced delirium with propranolol. Smart use included pindolol, especially in patients on antidepressants, because of add on efficacy, however we do not have long term trials. At the end I think cooperation between clinical pharmacist and psychiatrist and cardiologist is the best approach to deal with these patients.
The essential logic is to decrease the time of exposure to cardiovascular risk factors with genetic insights providing strong justification for this approach. Lifetime exposure to lower concentrations of cholesterol specifically, plasma levels of low-density lipoprotein (LDL) cholesterol, is shown to be associated with larger reduction in the risk of coronary heart disease. The decrease in risk is related to the genetic variants of receptors that remove cholesterol from the circulation matched with individuals who do not carry such variants. For a known reduction in LDL cholesterol, there was much more impact on reduction in cardiovascular disease risk than that reached with pharmacotherapeutic modulation in late life. Several studies have shown that the adoption of a healthy life , the act of not smoking, weight control and perform regular physical activity , with the reduction of cholesterol levels can be more effective than drug therapy of known effectiveness. How best to link these two strategies and show people that the protection of their coronary health goes beyond the use of drugs ?
Beyond the classic formula [MAP = DAP + 0.33 PP] ;
PP = systolic-diastolic pressure, DAP = diastolic arterial pressure
Can you suggest other formulas or methods for non-invasive estimation of mean arterial BP?
Some researchers showed evidence for using BNP as a prognostic indicator for individuals with HFPEF (Van Veldhuisen et al., 2013). Is there any other evidence or anecodotal advice on this matter? Thank you.
Van Veldhuisen D, Linssen G, Hillege H, et al. B-type natriuretic Peptide and prognosis in heart failure patients with preserved and reduced ejection fraction. Journal Of The American College Of Cardiology (JACC) [serial online]. April 9, 2013;61(14):1498-1506.
Type 2 CRS is defined as renal detoriation due to chronic heart failure. because of chronic fluid overload due to CHF, renal venose pressure is increased. thus glomerular filtration rate is decreased. if we use of dopamine in 2 mg/kg/min dosage, afferent arteriol would dilated and GFR would be increased. Is it like this indeed? is there anyone who had experience use of dopamine (2 mg/kg/min) in Type 2 Cardio Renal Syndrome?
The incidence of asymptomatic valvular lesions is very high and many of them require management based on echo findings.The positive and negative predictive values of cardiac clinical findings is also very poor.The students of cardiology miss out on diagnosis ,assessment of severity and management decisions in valvular heart disease.,A recent WHO report suggested that more than 50% of Rheumatic heart diseases are missed out even by experienced physicians.A lot of time is invested in teaching findings which have poor agreement and predictive values for UG and PG teaching.
Superficial Middle Cerebral Vein OR Basal Vein of Rosenthal both these venous drainages are rare in Carotido-Cavernous Fistula. But which one of these is more dangerous?
Thanks Professors in advance.
A sample link for Beginners here:
Rupture of ventricular septum, Papillary muscle and free ventricular wall after myocardial infarction in the same patient .Did your patient survive? Usually these patients don't survive.
Avastin can affect vascular permeability, normal BBB restrictions on Mg diffusion would thereby be bypassed opening the possibility of excitation and possibly seizures in those prone,
Can anybody explain association of Hypertension with High density lipoprotein, I am doing an analysis and the protective association is coming out between low levels of HDL with presence of hypertension.
What could be the possible explanation, is there any biological plausibility or any other explanation of this phenomenon.
Note: The sample size is adequate, the study is powered statistically and there is no misclassification. Multivariate analysis has also done appropriately with adjusting for potential confounders.