by Mark | Dec 20, 2016 | Uncategorized
Device Guidelines for Patients with Genetic Heart Disease: Pacemakers Permanent Pacemaker (2008 guidelines) Long QT Syndrome (LQTS) Class IIa Permanent pacing is reasonable for high-risk patients with congenital long-QT syndrome. Class III Permanent pacing is not indicated for frequent or complex ventricular ectopic activity without sustained VT in the absence of the long-QT syndrome. Hypertrophic Obstructive Cardiomyopathy (HoCM) Class I Permanent pacing is indicated for SND or AV block in patients with HCM as described previously. Class IIb Permanent pacing may be considered in medically refractory symptomatic patients with HCM and significant resting or provoked LV outflow tract obstruction. As for Class I indications, when risk factors for SCD are present, consider a DDD ICD Class III Permanent pacemaker implantation is not indicated for patients who are asymptomatic or whose symptoms are medically controlled. Permanent pacemaker implantation is not indicated for symptomatic patients without evidence of LV outflow tract obstruction. HOCM Guidelines (2011) Class IIa In patients with HCM who have had a dual-chamber device implanted for non-HCM indications, it is reasonable to consider a trial of dual-chamber atrial-ventricular pacing (from the right ventricular apex) for the relief of symptoms attributable to LVOT obstruction. Class IIb Permanent pacing may be considered in medically refractory symptomatic patients with obstructive HCM who are suboptimal candidates for septal reduction therapy. Class III: No Benefit Permanent pacemaker implantation for the purpose of reducing gradient should not be performed in patients with HCM who are asymptomatic or whose symptoms are medically controlled. Permanent pacemaker implantation should not be performed as a first-line therapy to relieve symptoms in medically refractory...
by Mark | Dec 13, 2015 | Cardiac Electrophysiology, Cardiology, General Public
What is AVNRT? Rapid beating of the heart can cause the sensation of palpitations, which are often described as fluttering, pounding, and beating sensations in the chest. Sometimes these palpitations are rapid enough to affect other parts of the body, and people with palpitations may also describe feelings of lightheadedness, fatigue, and shortness of breath. Occasionally, these palpitations are rapid enough to cause people to pass out (syncope), though this is rare. Rapid palpitations may come from the heart’s upper chambers, the atria, and in most cases, are not generally considered life threatening (although rare exceptions do exist). Alternatively, palpitations may come from the heart’s lower chambers, the ventricles, which in some cases may be life-threatening. Also, the natural electrical “bridge” between the atria and ventricles, the atrio-ventricular (AV) node, can be a common site of arrhythmias causing palpitations. The best way to start the diagnosis of the cause of palpitations is to have an electrocardiogram (ECG) read by a physician experienced in heart rhythm disorders. Supraventricular tachycardia (SVT) is a category of arrhythmias that come from above the ventricles. The most common type of regular SVT is AtrioVentricular Nodal Reentrant Tachycardia (AVNRT), and is responsible for 50% of SVT cases (1). AVNRT is more common in women than men, and typically occurs in patients between 20 and 40 years old. This long, descriptive arrhythmia name details the biology of the abnormal electrical circuit within the heart that leads to the palpitations that are commonly described. In AVNRT, there is a small circular (Reentrant) electrical circuit that “spins” around in the AV node, the normal, natural electrical bridge between the atria and ventricles....
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...
by Mark | Sep 23, 2015 | Cardiology
Indications for Nuclear Myocardial Perfusion Imaging (MPI): Exercise MPI: Intermediate-high risk, able to exercise, with uninterpretable ECG (class I) or interpretable ECG (class IIa) Known SIHD, able to exercise, new symptoms Contraindications to Exercise MPI: Low-risk & able to exercise –> instead do Exercise ECG Routine LV function if no new signs/symptoms No changes < 5 yr after ACB surgery or < 2 yr after PCI Essentially asymptomatic patients Pharmacological MPI: Intermediate-high risk and unable to exercise Left Bundle Branch Block (LBBB) regardless of exercise Known SIHD, unable to exercise or LBBB, new symptoms Contraindications to Pharma MPI: Low-risk & able to exercise –> instead do an Exercise ECG Intermediate-high risk, able to exercise, interpretable ECG –> instead do exercise ECG or MPI Routine LV function if no new signs/symptoms No changes < 5 yr after ACB surgery or < 2 yr after PCI Essentially asymptomatic patients Uninterpretable ECG, remember the mnemonic PELViS: P: pre-excitation (WPW) E: excess of > 1 mm ST depression L: left bundle branch block (LBBB) V: ventricular pacing i S: ST/T changes from LVH or digoxin for example Disclaimer © 2015 www.markmccauleymd.com. All rights served. ...
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