by Mark | Aug 28, 2019 | Cardiac Electrophysiology, Cardiology, General Public, Science
I am excited to announce that work from our laboratory was recently published in Circulation: Arrhythmia and Electrophysiology, as an Editor’s Choice Article. In this work, we show for the first time that the native electrical signal in the heart can be transferred from one region to another with a surgical suture made from carbon nanotube fibers (CNTf). The CNTf sutures have remarkable electrical conductivity, strength, and flexibility and are the first to be used in surgical applications to restore electrical conduction in the heart. The long-term impact of this work is that the reestablishment of cardiac conduction has the potential to revolutionize therapy for cardiac electrical disturbances, one of the most common causes of death in the United States. Link to the article can be found here: In Vivo Restoration of Myocardial Conduction with Carbon Nanotube Fibers. News media coverage can be found here: Physics World, Nanotechnology News, Phys.Org, Today’s Medical...
by Mark | Oct 1, 2015 | Cardiac Electrophysiology, Cardiology, Science
Indications for Pacemaker (Class I and IIa/b Recommendations) Sinus node dysfunction (SND) with symptomatic bradycardia Symptomatic chronotropic incompetence Required drug therapy causing symptomatic bradycardia SND with HR < 40 bpm; bradycardia and symptom connection unclear Unexplained syncope and EP study (+) for SND Conisder for minimal symptoms but HR < 40 bpm while awake Type II second-degree AV block, or complete third-degree AV block with: Bradycardia + symptoms Arrhythmias + required bradycardic meds Asymptomatic awake with pauses > 3 sec, Asymptomatic awake with v-rate < 40 bpm, Asymptomatic awake with infra-His conduction Asymptomatic awake with AF and > 5 sec pauses After catheter ablation of AV junction Post-operative AVB not expected to resolve Neuromuscular: myotonic dystrophy, Kearns-Sayre, Erb dystrophy, peroneal muscular atrophy Symptomatic bradycardia + second-degree AVB Asymptomatic bradycardia + type II second-degree AVB (narrow or wide QRS) Asymptomatic second-degree AVB at intra or infra His level on EP study Asymptomatic complete third-degree AVB with: V-rate < 40 bpm LV dysfunction Site of block below AV node Reasonable in V-rate > 40 and persistent First or Second Degree AVB with: Pacemaker syndrome Hemodynamic compromise Muscular dystrophy of any AV block, with or without symptoms Recurrence of AVB is expected after offending drug is withdrawn Advanced second-degree AVB or third-degree AVB Type II 2nd degree AVB Alternating Bundle Branch Block Syncope of unknown type after exclusion of other causes including VT HV > 100 msec, even if asymptomatic EP study with infra-Hisian block, even if non-physiological After STEMI with: persistent 2nd/3rd DAVB regardless of symptoms, transient infranodal AVB Carotid sensitivity causing syncope and ventricular asystole > 3 sec Hypersensitive cardioinhibition >...
by Mark | Sep 29, 2015 | Cardiology, Science
Constrictive Pericarditis Pathology of constriction: Thick scarred pericardium equalizes 4 chamber pressure, limits ventricular filling, reduces cardiac volume. JV pressure wave form in constriction: rapid ventricular (RV) filling causes rapid Y-descent Then, diastolic filling stops abruptly, causing a dip and plateau diastolic RV waveform Causes of constriction: Mediastinal radiation Chronic idiopathic pericarditis Cardiac surgery Tuberculous pericarditis Signs & Symptoms of Constriction: R-sided heart failure: JVD, hepatic congestion, ascites, peripheral edema Clear lungs Exercise intolerance, muscle wasting, cardiac cachexia Jugular veins with prominent X and Y descent Y descent may look like JV pulse is “falling away” from you Respiratory increase in jugular venous pressure (Kussmaul’s sign) Pericardial knock (high-pitched early diastolic sound) Imaging of Pericardial Constriction: CT with thickening +/- calcification of the pericardium CT/MRI preferred modalities to evaluate pericardial thickening Echo may show systolic discordance of LV/RV pressures, ventricular interdependence In constriction, cath of LV and RV will show discordance of LV and RV pressures Differential Diagnosis of Pericardial Constriction: Restrictive cardiomyopathy RCM and Constriction both have Kussmaul’s sign, RV cath “dip and plateau” sign in early diastole Whereas RCM has no significant respiratory mitral variation, Constriction has marked variation of mitral inflow (>25%) and hepatic flow Whereas RCM has early reduced diastolic mitral annular velocity (Ea), Constriction has normal Ea velocities Whereas RCM is associated with pulmonary congestion, Constriction usually has clear lungs Whereas RCM has a reduced mitral annular diastolic velocity < 8 cm/s, Constriction has mitral annular diastolic velocity > 8 cm/s Whereas RCM shows ventricular concordance on simultaneous LV/RV cath, Constriction has ventricular discordance on simultaneous LV/RV cath Cardiac Tamponade Constriction and Tamponade both have elevated JVP, Kussmaul’s sign, pulsus...
by Mark | Sep 29, 2015 | Cardiology, Science
Pheochromocytoma vs. Carcinoid – What’s the Difference?? Two neuroendocrine tumors affecting the cardiovascular system and often get confused are carcinoid and pheochromocytoma. I thought I would include a brief primer on the two, because both secrete some degree of catecholamines; however both are completely different in management and treatment. Carcinoid Primarily secretion of serotonin (5-HT) >> catecholamines Serotonin release: flushing, diarrhea, bronchospasm/wheezing, Carcinoid heart disease Tumors found in midgut enterochromaffin cells: small intestines, cecal, ascending colon, bronchopulmonary. Happens in 5th to 7th decade of life usually. Serotonin cycle in Carcinoid: tryptophan –(trp-OH-ase)—> 5OH-tryptophan —(AADC)–> serotonin —(MAO)–> 5-HIAA The serotonin metabolite 5-HIAA is excreted in urine and is used to diagnose Carcinoid. 24-hour urine 5-HIAA is the most important clue to Carcinoid syndrome. Carcinoid heart disease: tricuspid regurgitation with TV “frozen” midway, pulmonary stenosis > regurgitation, R>L HD, increased PFO incidence, prominent early large “v” wave in jugular veins. False-positive Ur-5-HIAA: high tryptophan diet False-negatve Ur-5-HIAA: levodopa therapy for Parkinson’s Medical therapy for Carcinoid: Octreotide (somatostatin analogue), reduces vasoactive peptide secretion. Surgical therapy for non-metastatic Carcinoid: surgical resection —————————————————————————————————————————————————- Pheochromocytoma Primarily catecholamine release >> serotonin release. Pheo catecholamines are released from the adrenal medulla (85%) or extra-adrenal chromaffin tissue (15%) Classic symptoms of Pheo: episodic hypertension, palpitations, sweating, headache, orthostatic BP, vasoconstriction, anxiety/panic. Metabolic Pheo Sequelae: hyperglycemia, lactic acidosis, weight loss Associated with genetic conditions: MEN2, VHL, NF1, and SDH B/D Remember, MEN2 = MTC, Pheo, PTH (2a) or mucosa neuroma (2b) Pheo (bio)chemical diagnosis: plasma-free metanephrines, urinary fractionated metanephrines Reason: catecholamines produced by pheo are metabolized to metanephrines, independent of quantity of pheo release Pheo imaging: CT/MRI, I123-MIBG imaging Surgical Pheo...
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