In CHF, when should Metformin be avoided?
Severe of decompensated - risk of lactic acidosis
Glitazones should avoided in patients with Class III or IV sx
Which group of CHF is most at risk of hyperkalemia from dual ACE/ARB therapy?
Patients with diabetes, in whom hyporeninaemic hypoaldosteronism is common, may be at risk of developing hyperkalaemia when an angiotensin II receptor antagonist is added to ACEI therapy, and vigilant monitoring of serum potassium is recommended.
What is the thromboembolism risk of CHF patients?
There is evidence that CHF is associated with an increased risk of thromboembolism (e.g. because of the frequent presence of thrombi within akinetic segments of failing ventricle and an increased propensity to develop AF). The SOLVD trial clearly demonstrated an increase in the incidence of stroke (mainly thromboembolic) with decreasing ventricular function.
However, retrospective analyses of studies of anti- thrombotic therapy in CHF have yielded conflicting results.
How is gout managed in CHF?
Plasma urate goes up in CHF and levels have adverse prognostic significance
Can't have NSAIDs or Cox-2sCan't have steroids
Xanthine oxidase inhibition does not demonstrate benefits on clinical outcomes
In what arrhythmias is EPS not indicated?
The value of electrophysiology studies is greatest in patients who are suspected of having a tachyarrhythmia whose mechanism is reentry.
There is no role for electrophysiology studies in the evaluation or management of the long QT syndrome, catecholaminergic polymorphic ventricular tachycardia, or the short QT syndrome.
What are the diagnostic indications of EPS?
Underlying ischemic or structural heart disease to see if underlying sustained ventricular arrhythmias or congenital tachyrrhtyhmias may be the cause
Inappropriate sinus bradycardia due to suspected sick sinus syndrome (prolonged corrected SA node recovery may predict future syncope recurrence)
Bifascicular, or LBBB/RBBB + hemifasciular block of unknown cause. Induction of infra-Hisian block with bifasci block can predict future adverse cardiovascular events
Patients with high risk occupations
Sudden cardiac death with no established cause (presumed idiopathic VF)
Wide complex tachyarrythmias of unclear etiology on noninvasive measures
What are the risk stratification indications for EPS?
Previous MI with ischemic cardiomyopathy who have LVEF<40% and found to have nonsustained VT/VT on ambulatory monitoring
AV conduction block below the level of the AV node (Mobitz II is infranodal which is bad) - EP is used when you can't work out the site of block in an asymptomatic individual. If infranodal --> pacemaker.
Asymptomatic young (8-21 years) with ECG manifestations of pre-excitation - risk of sudden cardiac death from atrial arrhythmia progressing to ventricular. Need EST first and if loss of pre-excitation is NOT seen --> EP
Screening test for those with TOF who do not have high risk factors, or in patients with prepared TOF
Controversial in Brugada, can be used for risk stratification with cardiac sarcoid if LVEF <35 despite optimal medical therapy and immunosuppression
What are the absolute contraindications to EPS?
Unstable angina●Bacteremia or septicemia●Acute decompensated congestive heart failure not caused by the arrhythmia●Major bleeding diathesis●Acute lower extremity venous thrombosis if femoral vein cannulation is desired
Where is the value of EP studies the greatest?
It would also be important to realize that the value of electrophysiology studies is greatest in patients who are suspected of having a tachyarrhythmia whose mechanism is reentry. There is no role for electrophysiology studies in the evaluation or management of the long QT syndrome, catecholaminergic polymorphic ventricular tachycardia, or the short QT syndrome.
In Mobitz II block, when is pacing indicated?
An EP study is indicated if the site of block cannot be determined reliably in an asymptomatic individual with second degree AV block. If the site is infranodal, pacing is indicated
What is the risk with young people and pre-excitation syndromes?
Asymptomatic young (8 to 21 years) patients with electrocardiographic manifestations of preexcitation may be at high risk of sudden cardiac death due to atrial fibrillation progressing to ventricular fibrillation. These patients are advised to undergo exercise stress testing. The clear and sudden loss of preexcitation with exercise stress testing predicts a favorable prognosis. If clear loss of preexcitation is not seen or the data are uninterpretable, invasive risk stratification via transesophageal or EP studies is recommended
What are the annual risk factors of untreated stroke?
CHADS risk factors are cumulative
< 65 years with no risk factors the untreated annual risk of stroke is about 1%, whereas with one or more risk factors it is about 5%;
65-75 years with no risk factors the annual risk of stroke is about 4%, and with one or more risk factors it is about 6% per year;
>75 years with no risk factors the risk of stroke is about 3%-4%, whereas with one or more risk factors it is about 8%
In patients who receive thrombolysis and are later found to have a total occlusion of a vessel on angio - should they get stented?
If asymptomatic - NO, medical therapy has better effect on cardiovascular remodelling than PCI
If symptomatic (i.e. angina or poor stress testing results) then YES
How long after thrombolysis should angio be performed?
ASAP but AFTER 2 hours if high risk features: anterior MI, killip class >2, inferior MI w/ RV involvement, BP <100, HR > 100
Not high risk, should be performed within 24 hours
What is the difference between primary failure of fibrinolysis and threatened reocclusion?
Primary failure - evidence of continuing or worsening myocardial ischemia
Threatened reocclusion - early recurrent ischemia after apparently successful fibrinolysis
In a patient who undergoes fibrinolysis for MI, when would you consider re-thrombolysing?
In patients with both primary failure and threatened reocclusion - PCI is preferable.
In PCI can't be done within two hours, for threatened reocclusion, thrombolysis with a non-antigenic agents should be done.
For primary failure, if rescue PCI can't be performed within 12 hours, conservative care wins over thrombolysis
Which group of patients should get a bare metal stent?
Patients in whom a DES cannot be implanted for technical reasons
Patients for whom compliance with a recommendation for 12 months of dual antiplatelet therapy is likely to be problematic, including those known to have difficulty with medication compliance.
Those who are scheduled to undergo surgery requiring cessation of dual antiplatelet therapy in the ensuing year
Those known to be at higher risk of bleeding, including individuals taking an oral anticoagulant.
How long after PCI should you continue dual antiplatelet therapy for?
For patients treated with either DES or BMS who are not at high bleeding risk and who do not have planned noncardiac surgery within one year, we recommend DAPT for at least 12 months rather than a shorter treatment duration (Grade 1B). Practitioners should evaluate patients after the first 12 months of DAPT to be certain that there has not been major bleeding or other important difficulty related to DAPT. For patients who have had a complication of DAPT, continuation after 12 months may not be appropriate
A patient has a DES and completes 12 months of dual antiplatelet therapy with no complications - how long should you continue it for?
For patients who have not had a significant complication with DAPT during the first 12 months, we suggest continuing such therapy for an additional 18 months (Grade 2B).
How long should you continue dual antiplatelet for in a high risk patient with a BMS?
For patients treated with BMS at high bleeding risk or who have planned noncardiac surgery within one year, we recommend a minimum of one month of uninterrupted DAPT (Grade 1B). For such patients treated with DES, we recommend uninterrupted DAPT for a minimum of six months
When should you use clopidogrel over ticagrelor or prasugrel?
In most randomized trials of stent placement for stable coronary artery disease, clopidogrel was the P2Y12 receptor blocker tested. Thus, we prefer clopidogrel to prasugrel or ticagrelor for most patients requiring dual antiplatelet therapy.
When is Prasugrel used?
Prasugrel, co-administered with aspirin, has proven benefit in:
prevention of atherothrombotic events in patients with acute coronary syndromes (unstable angina, non–ST elevation myocardial infarction, ST elevation myocardial infarction) who are to undergo percutaneous coronary intervention.
What are the considerations with Ticagrelor and Prasugrel?
A higher risk of bleeding may be seen when prasugrel is used for patients weighing less than 60 kg or aged 75 years or more. It should be avoided or used with extreme caution in these patients.
Ticagrelor should be avoided or used with extreme caution in patients at high risk of bleeding, such as those with low body weight (less than 60 kg), reduced kidney function and of older age (65 years or more).
What are the Glycoprotein IIB/IIA inhibitors?
Abciximab, eptifibatide and tirofiban block platelet aggregation by preventing binding of fibrinogen to platelets through blockade of the platelet glycoprotein IIb/IIIa receptor. These drugs should only be used under specialist supervision.
How do GPIIb/IIIa inhibitors work?
Inhibit the final common pathway of platelet aggregation, the cross-bridging of platelets secondary to fibrinogen binding to the activated GP IIb/IIIa receptor. The addition of GP IIb/IIIa improves outcomes in some patients with non-ST elevation ACS.
What is the most important risk factor for stent thrombosis?
The premature cessation of dual antiplatelet therapy is the most important risk factor for ST.
How does stent restenosis present?
Stable coronary sx as opposed to acute and dynamic
What is the difference between stent thrombosis and stent restenosis?
Restenosis is a gradual re-narrowing of the stented segment that occurs mostly between 3 to 12 months after stent placement. It usually presents as recurrent angina but can present as acute myocardial infarction in approximately 10 percent of patients. It can usually be managed by repeat percutaneous revascularization.
In contrast, stent thrombosis is an abrupt thrombotic occlusion of a previously widely patent stent. It is a catastrophic complication that presents as sudden death or large myocardial infarction in most patients. Despite successful repeat revascularization, the six-month mortality is high.
In what acute MI setting would you use beta-blockers immediately?
Failed thrombolysis with preserved blood pressure and tachycardia - aim is to get HR <70 while maintaining systolic BP >90
Why is amitriptyline so cardiotoxic?
As well as being an SNR it is also a sodium channel blocker and an L-type calcium channel blockerr