Category: Cardiology
Posted: 12/28/2014 by Semhar Tewelde, MD
Click here to contact Semhar Tewelde, MD
Holiday Heart
- Holiday heart commonly refers to alcohol use and rhythm disturbances, particularly supraventricular tachydysrhythmias.
- The most common rhythm disorder is atrial fibrillation (AF), which usually converts to normal sinus rhythm within 24 hours and antiarrhythmic therapy is typically not indicated.
- Analyses of ECGs in patients who have consumed a large quantity of alcohol show prolongation of the PR, QRS, and QT intervals.
- 2014 AHA/ACC/HRS updated guidelines for nonvalvular AF utilize the CHA2DS2-VASc (congestive heart failure, hypertension, age ≥75 years [doubled], diabetes mellitus, prior stroke or TIA or thromboembolism [doubled], vascular disease, age 65 to 74 years, and sex category) score for assessment of stroke risk.
Tonelo D, Providência R, Gonçalves L. Holiday heart syndrome revisited after 34 years. Arq Bras Cardiol. Aug 2013;101(2):183-9.
2014 AHA/ACC/HRS Guideline for the Management of Patients with Atrial Fibrillation: Executive Summary. JACC Vol 64, Issue 21, Dec 2014.
Category: Cardiology
Keywords: Brugada (PubMed Search)
Posted: 12/21/2014 by Semhar Tewelde, MD
(Updated: 1/19/2015)
Click here to contact Semhar Tewelde, MD
Brugada Syndrome
Brugada syndrome is an inherited arrhythmogenic channelopathy described by ST-segment elevation in the right precordial leads and an increased risk of sudden cardiac death.
There are 3 electrocardiographic patterns:
Type 1 – Coved morphology w/ST-elevation >2 mm, followed by a negative T wave in at least 1 right precordial lead
Type 2 - Saddleback morphology w/ST-elevation >2mm, with a positive or biphasic T wave
Type 3 - Either coved, or saddleback morphology with <2mm ST-elevation
Type 1 pattern is often underestimated because of its sporadic/fluctuating appearance on ECG, which can be either spontaneously occurring or drug-induced (drug-induced variant has a more favorable prognosis).
Fever has been a well-documented culprit in unmasking Brugada pattern by increasing the sodium channel dysfunction & accelerating the late sodium current inactivation.
A recent study in a large population of patients with type 1 Brugada attempted to identify other patterns unmasking Brugada using 24-hour holter monitoring. * There is now evidence that there is a higher prevalence of type 1 Brugada pattern from 12pm-6pm & unmasking by fast and a large meal, showing influence by glucose intake and insulin levels.
Cerrato N, Giustetto C, et al. Prevalence of Type 1 Brugada Electrocardiographic Pattern Evaluated by Twelve-Lead Twenty-Four-Hour Holter Monitoring. The American Journal of Cardiology.Vol 115, Issue 1, 1 Jan. 2015, pgs. 52-56.
Category: Cardiology
Posted: 12/14/2014 by Semhar Tewelde, MD
Click here to contact Semhar Tewelde, MD
Not So Benign: Benign early repolarization (BER) effects in STEMI
- Benign early repolarization (BER) has been associated with increased risk of sudden cardiac death and ventricular fibrillation (VF) in patients with and without structural heart disease.
- Acute STEMI is associated with high incidence of ventricular arrhythmias and the most frequent cause of sudden cardiac death in the adult population.
- BER has been associated with arrhythmogenicity, however the prognostic importance of this ECG finding in patients with STEMI has not been well elucidated.
- In a recent prospective study of STEMI patients, BER was associated with higher rates of in-hospital ventricular arrhythmias and mortality; It is an independent predictor of long-term mortality beyond well-known other parameters.
Ozcan K, et al. Presence of early repolarization on admission electrocardiography is associated with long-term mortality and MACE in patients with STEMI undergoing primary percutaneous intervention. Journal of Cardiology, Volume 64, Issue 3, September 2014, Pages 162-163.
Category: Cardiology
Posted: 12/7/2014 by Semhar Tewelde, MD
Click here to contact Semhar Tewelde, MD
Predictors of Cardiac Rupture After AMI
- In the era of revascularization and aggressive cardiac care there has been a continual decline in acute myocardial infarction (AMI) mortality rates; however one of the most deadly complications, cardiac rupture (left ventricular free wall, ventricular septum, or papillary muscle rupture), still remains relatively stable.
- Cardiac rupture is an increasingly more frequent cause of death during AMI, thus a recent study retrospectively assessed the clinical and morphologic variables in those with and without cardiac rupture that were hospitalized for AMI.
- Cardiac rupture overwhelmingly complicates a first AMI.
- Cardiac rupture occurs most often in patients with an immense quantity of cardiac adipose tissue, the size of the left ventricular cavity is typically normal, and the area of the infarct is small.
- Heart failure patients with prior AMI have healed scar tissue and are at nominal risk of complications such as rupture if a subsequent AMI occurs.
Roberts W, et al. Commonalities of Cardiac Rupture (Left Ventricular Free Wall or Ventricular Septum or Papillary Muscle) During Acute Myocardial Infarction Secondary to Atherosclerotic Coronary Artery Disease. The American Journal of Cardiology. Volume 115, Issue 1, Pages 125-140 (1 January 2015).
Category: Cardiology
Keywords: Patent Foramen Ovale (PubMed Search)
Posted: 11/23/2014 by Semhar Tewelde, MD
(Updated: 11/21/2024)
Click here to contact Semhar Tewelde, MD
Patent Foramen Ovale: To Close or Not to Close
- Patent foramen ovale (PFO) is associated with a 3-fold increased risk for recurrent stroke, yet current guidelines only recommends “consideration” of PFO closure after a second cryptogenic stroke.
- Studies have demonstrated reductions in recurrent neurologic events with transcatheter PFO closure compared with medical therapy alone.
- Until recently the cost-effectiveness of PFO closure has not been described.
- Although PFO closure was found to be immediately more costly per patient closure, it reached cost-effectiveness at ~2.5 years of follow-up.
- Closure of PFO is both beneficial in terms of risk-benefit and cost-effectiveness strategy, especially as cryptogenic stroke typically affects the young.
Pickett C, Villines T, Ferguson M, et al. Cost Effectiveness of Percutaneous Closure Versus Medical Therapy for Cryptogenic Stroke in Patients With a Patent Foramen Ovale. The American Journal of Cardiology. Volume 114, Issue 10, Pages 1584-89 (15 November 2014)
Category: Cardiology
Posted: 11/9/2014 by Semhar Tewelde, MD
(Updated: 11/21/2024)
Click here to contact Semhar Tewelde, MD
Coronary Subclavian Steal Syndrome
Coronary subclavian steal syndrome (CSSS) is defined as coronary ischemia resulting from the reversal of flow in an internal mammary arterial graft usually secondary to subclavian stenosis.
Angiographic subclavian stenosis is defined as greater than 50% narrowing or greater than 20mmHg pressure difference across a lesion.
CSSS occurs in up to 4.5% of patients with prior CABG & common in older individuals with existing peripheral vascular disease.
CSSS most commonly manifests as stable angina, but frequently presents as unstable angina, acute myocardial infarction, acute systolic heart failure or even cardiogenic shock.
Screening for subclavian stenosis prior to CABG w/bilateral noninvasive blood pressure assessment, and a 15 mmHg or greater discordance should elicit further imaging.
Percutaneous revascularization is the first-line therapy for CSSS and has excellent long-term outcomes.
Sintek M, Coverstone E, Singh J. Coronary Sunclavian Steal Syndrome. Current Opinion in Cardiology. Issue: Volume 29(6) pgs. 506-513 November 2014.
Category: Cardiology
Posted: 11/2/2014 by Semhar Tewelde, MD
Click here to contact Semhar Tewelde, MD
Heart Failure & Pulmonary Hypertension (Part II)
- HFpEF-PH management guidelines recommend the treatment of symptoms of congestion and volume overload, targeting LV relaxation and co-morbidities; including the management of pulmonary congestion, ischemia, sleep apnea, atrial fibrillation, and diabetes.
- Both atrial/ventricular dysrhythmias contribute to the mortality associated with HF & control of particularly atrial fibrillation, is an essential part of the early pulmonary vascular remodeling process.
- Both endothelin receptor antagonists (ERA) and prostanoids have been effective for PAH & clinical trials utilizing these agents have also been attempted in treatment of PH due to left heart disease, but have proven to be either neutral or even detrimental.
- Selective dilation of the pulmonary vessels in patients with postcapillary PH, without simultaneously ensuring the unloading of the LV, can cause profound pulmonary venous congestion resulting in sudden pulmonary edema, which greatly increases the morbidity in patients with this form of PH.
- Currently, the most compelling published data for pharmacological treatment targeting PH in HFpEF involves phosphodiesterase (PDE) inhibitor sildenafil.
Kanwar M, Tedford R, et al. Management of Pulmonary Hypertension due to Heart Failure with Preserved Ejection Fraction. Current Hypertension Reports. October 16, 2014.
Category: Cardiology
Posted: 10/26/2014 by Semhar Tewelde, MD
(Updated: 11/21/2024)
Click here to contact Semhar Tewelde, MD
Heart Failure & Pulmonary Hypertension (Part I)
~50% of patients with heart failure & preserved ejection fraction (HFpEF) develop pulmonary hypertension (PH)
HFpEF with PH portends reduced survival and increased hospitalization rates compared to those without PH
HFpEF-PH is often confused with idiopathic pulmonary hypertension (IPAH) given the similar hemodynamics; differentiating them is challenging and requires careful consideration of clinical, radiologic, and hemodynamic data
| PAH | HFpEF |
Clinical parameters: | ||
Age | Typically 3rd–5th decade | Typically 6th–8th decade |
Comorbidities (HTN, HLD, DM, CAD) | Rare | Common |
Atrial arrhythmias | Rare | Common |
Obstructive sleep apnea | Rare | Common |
Echocardiographic parameters: | ||
LA size/volume | Normal | Increased |
LV diastolic function | Normal to mildly abnormal | Moderate to severely abnormal |
Hemodynamic parameters: | ||
Resting PAWP | Always <15 mmHg | May be < or >15 mmHg |
Response to volume | PAWP <15 mmHg (increase ≤5 mmHg) | PAWP >15 mmHg (increase >5 mmHg) |
Response to exercise | PAWP <15 mmHg (increase ≤5 mmHg) | PAWP >15 mmHg (increase >5 mmHg) |
(Table reproduced from article)
Kanwar M, Tedford R, et al. Management of Pulmonary Hypertension due to Heart Failure with Preserved Ejection Fraction. Current Hypertension Reports. October 16, 2014
Category: Cardiology
Posted: 10/19/2014 by Semhar Tewelde, MD
Click here to contact Semhar Tewelde, MD
Cardiovascular Morbidity & Sleep Apnea
Obstructive sleep apnea (OSA) is characterized by sleep-related periodic breathing, upper-airway obstruction, sleep disruption, and hemodynamic perturbations
Epidemiological data shows a strong association between untreated OSA & cardiovascular morbidity/mortality
Two recent studies by Gottlieb et al. (1) & Chirinos et al. (2) elucidated two important explicit and complicit treatment considerations for OSA
(1) In moderate-to-severe obstructive sleep apnea, the use of CPAP alone during sleep may ameliorate systemic hypertension and cardiovascular risk, even in patients who do not have "subjective" sleepiness
(2) Weight loss combined with CPAP use may further decrease cardiovascular morbidity
Basner R. Cardiovascular Morbidity and Obstructive Sleep Apnea. N Engl J Med 2014; 370:2339-2341 June 12, 2014
Category: Cardiology
Posted: 10/12/2014 by Semhar Tewelde, MD
(Updated: 11/21/2024)
Click here to contact Semhar Tewelde, MD
Kounis Syndrome (Part II)
- KS can develop from multiple etiologies: hymenoptera, proteins, vasoactive amines, histamine, acetylcholine, multiple antibiotics, and various medical conditions (angioedema, serum sickness, asthma, stress-induced cardiomyopathy).
- Hypersensitivity myocarditis and KS are two cardiac entities of allergic etiology affecting the myocardium and coronary arteries, respectively. These two entities can mimic each other and can be clinical indistinguishable.
- Presence of eosinophil’s, atypical lymphocytes, and giant cells on myocardial biopsy suggests hypersensitivity myocarditis.
- There is evidence showing use of corticosteroids with vasospastic angina with evidence of allergy or the presence of symptoms refractory to high-dose vasodilators has been reported to resolve symptoms.
Kounis GN, Soufras GD, Kouni SA, et al. Hypersensitivity myocarditis and hypersensitivity coronary syndrome (Kounis syndrome). Am J Emerg Med 2009;27:506–508.
Vivas D, Rubira JC, Ortiz AF, et al. Coronary spasm and hypersensitivity to amoxicillin: Kounis or not Kounis syndrome? Int J Cardiol 2008;128:279–281.
Category: Cardiology
Posted: 10/4/2014 by Semhar Tewelde, MD
Click here to contact Semhar Tewelde, MD
Kounis Syndrome (Part I)
- Kounis & Zavras (1991) described the syndrome of allergic angina and allergic myocardial infarction, currently known as Kounis syndrome (KS). Braunwald (1998) noted vasospastic angina can be induced by allergic reactions, with mediators such as histamine and leukotrienes acting on coronary vascular smooth muscle.
- Two subtypes have been described: type I, occurring in patients without predisposing factors for CAD often caused by coronary artery spasm and type II, occurring with angiographic evidence of coronary disease when the allergic events induce plaque erosion or rupture.
- This syndrome has been reported in association with a variety of medical conditions, environmental exposures, and medication exposures. Entities such as Takotsubo cardiomyopathy, drug-eluted stent thrombosis, and coronary allograft vasculopathy also appear to be associated with this syndrome.
- Clinical presentation includes: symptoms and signs of an allergic reaction and acute coronary syndrome: chest pain, dyspnea, faintness, nausea, vomiting, syncope, pruritus, urticaria, diaphoresis, pallor, palpitations, hypotension, and bradycardia.
Kounis GN, Kounis SA, Hahalis G, et al. Coronary artery spasm associated with eosinophilia: another manifestation of Kounis syndrome? Heart Lung Circ 2009;18:163–164.
Mytas DZ, Stougiannos PN, Zairis MN, et al. Acute anterior myocardial infarction after multiple bee stings. A case of Kounis syndrome. Int J Cardiol 2009;134:e129–e131.
Category: Cardiology
Posted: 9/28/2014 by Semhar Tewelde, MD
(Updated: 11/21/2024)
Click here to contact Semhar Tewelde, MD
Ventricular Arrhythmias Originating from the Moderator Band
- Ventricular arrhythmias originating from the moderator band (MB) often have a distinct morphology
- Typically MB arrhythmias have a left bundle branch block pattern, QRS with a late precordial transition (>V4), a rapid down stroke of the QRS in the precordial leads, and a left superior frontal plane axis
- MB arrhythmias are often associated with PVC-induced ventricular fibrillation
- Catheter ablation is quite effective at termination of the arrhythmias and facilitated with intracardiac echocardiography (ICE)
Sadek M, Benhayon D, et al. Idiopathic ventricular arrhythmias originating from the moderator band: Electrocardiographic characteristics and treatment by catheter ablation. Heart Rhythm. Aug 2014
Category: Cardiology
Posted: 9/14/2014 by Semhar Tewelde, MD
Click here to contact Semhar Tewelde, MD
Optimal Revascularization in Complex Coronary Artery Disease
- A multicenter trial 4,566 patients with NSTEMI, unstable angina, and multi-vessel coronary artery disease were enrolled comparing outcomes of cardiac stenting versus coronary artery bypass.
- Cardiac stenting was associated with improved outcomes and lower mortality in the following subgroups: age >65 years, women, unstable angina, TIMI score >4, and 2 vessel disease.
- Despite high clinical risk patients who underwent cardiac stenting compared to surgical revascularization did better in this prospective registry.
Buszman P, Buszman P, Bochenek A, et al. Comparison of Stenting and Surgical Revascularization Strategy in Non-ST Elevation Acute Coronary Syndromes and Complex Coronary Artery Disease (from the Milestone Registry). JACC Oct 2014 Vol 114, Issue 7, pages 979-987.
Category: Cardiology
Posted: 9/7/2014 by Semhar Tewelde, MD
Click here to contact Semhar Tewelde, MD
PARADIGM Shift in Heart Failure
- Angiotensin-converting enzymes inhibitors (ACE-I) are cornerstone for treatment of heart failure (HF) given the multiple trials which have shown their positive risk reduction in cardiovascular death.
- Studies looking at the effect of angiotensin-receptor blockers (ARBs) on mortality have been inconsistent; thus ARB's have been recommended as 2nd-line for those who have unacceptable side effects to ACE-I.
- A recent double-blinded RCT (PARADIGM-HF) ~8400 patients with class II-IV HF w/ ejection fraction <40% were treated with enalapril (standard therapy) versus novel therapy with neprilysin (neutral endopeptidase) inhibitor combined with an ARB.
- Primary outcomes were death from cardiovascular causes and hospitalization for HF; The RCT was ceased early (~27 months) because of an overwhelming benefit with the new agent.
- At study closure death occurred 26.5% in the standard group versus 21.8% in the novel group. The risk of HF hospitalization was decreased 21% with novel therapy.
- In early studies the use of a neprilysin inhibitor combined with an ARB has shown superior effects to current standard therapy (ACE-I), however long-term effects of this novel therapy are yet to be determined.
McMurray J, Packer M, Desai A, et al. Angiotension-Neprilysin Inhibition versus Enalapril in Heart Failure. NEJM August 30, 2014.
Category: Cardiology
Keywords: Sick Sinus Syndrome (PubMed Search)
Posted: 8/31/2014 by Semhar Tewelde, MD
Click here to contact Semhar Tewelde, MD
Sick Sinus Syndrome
- Sick sinus syndrome (SSS) is a cardiac conduction disorder characterized by symptomatic dysfunction of the sinoatrial (SA) node.
- SSS usually manifests as sinus bradycardia, sinus arrest, or sinoatrial block, and is sometimes accompanied by supraventricular tachydysrhythmias.
- Symptoms of SSS include: syncope, dizziness, palpitations, exertional dyspnea, fatigability from chronotropic incompetence, heart failure, and angina.
- Clinically significant SSS typically requires pacemaker implantation. Approximately 30% to 50% of pacemaker implantation in the United States list SSS as the primary indication.
- 2 large, prospective cohorts with an average follow-up of 17 years, observed the incidence of SSS increases with age, does not differ between men and women, and is lower among blacks than whites.
- Risk factors for SSS included greater BMI & height, elevated NT-proBNP level & cystatin C level, longer QRS interval, lower heart rate, hypertension, and right bundle branch block.
Jensen P, Gronroos N, et al. Incidence of and Risk Factors for Sick Sinus Syndrome in the General Population. Journal of the American College of Cardiology. Vol 64 Issue 6, pages 531-538
Category: Cardiology
Keywords: GRACE score (PubMed Search)
Posted: 8/24/2014 by Semhar Tewelde, MD
(Updated: 11/21/2024)
Click here to contact Semhar Tewelde, MD
GRACE Score
- The Global Registry of Acute Coronary Events (GRACE) is an international database tracking outcomes of patients presenting with acute coronary syndromes (ACS).
- GRACE score is calculated based on 8 variables: Age, HR, systolic BP, creatinine, killip class, ST-segment deviation on EKG, cardiac biomarkers, and cardiac arrest on admission.
- Several reports have shown that the GRACE score is a better predictor of clinical outcome (risk of death or the combined risk of death or myocardial infarction at 6 months) than the TIMI score.
- A recent study evaluated the relationship between GRACE score & severity of coronary artery disease (CAD) angiographically evaluated by Gensini score in patients with NSTE-MI.
- Results showed that the GRACE score has significant relation with the extent & severity of CAD as assessed by angiographic Gensini score.
- GRACE score was shown to be important both for determining the severity of the CAD and predicting death within 6 months of hospital discharge from NSTE-MI.
Cakar M, Sahinkus S, et al. Relation between the GRACE score and severity of atherosclerosis in acute coronary syndrome. Journal of Cardiology. 2014 Vol 63, Issue 1, Pgs 24-28.
Category: Cardiology
Keywords: Nonatherosclerotic Coronary Artery Disease (PubMed Search)
Posted: 8/17/2014 by Semhar Tewelde, MD
(Updated: 11/21/2024)
Click here to contact Semhar Tewelde, MD
Nonatherosclerotic Coronary Artery Disease
- Nonatherosclerotic coronary artery disease (NACAD) is a term used to describe a category of diseases, which include: spontaneous coronary artery dissection (SCAD), coronary fibromuscular dysplasia (FMD), ectasia, vasculitis, embolism, vasospasm, or congenital anomaly.
- NACAD is an important cause of myocardial infarction (MI) in young women, but is often missed on coronary angiography.
- A small retrospective study of women <50 years of age with ACS found that 54.8% had normal arteries, 30.5% atherosclerotic heart disease (ACAD), 13% nonatherosclerotic coronary artery disease (NACAD), and 1.7% unclear etiology.
- NACAD accounted for 30% of MI’s with SCAD & Takotsubo cardiomyopathy accounting for the majority of cases.
Saw J, Aymong E, et al. Nonatherosclerotic Coronary Artery Disease in Young Women. Canadian Journal of Cardiology. 2014/07 Vol 30:Issue 7, pgs 814-819.
Category: Cardiology
Posted: 8/10/2014 by Semhar Tewelde, MD
Click here to contact Semhar Tewelde, MD
- Toxic effects of tricyclic antidepressants (TCA) are result of the following 4 pharmacologic properties:
1. Inhibition of norepinephrine & serotonin reuptake --> resultant seizure
2. Anticholinergic activity --> resultant altered mental status, tachycardia, mydriasis, ileus
3. Direct alpha-adrenergic blockade --> resultant hypotension
4. Cardiac myocyte sodium channel blockade --> resultant widened QRS
- A QRS interval greater than 100 milliseconds has ~30% chance of developing seizures and ~15% chance of developing a life-threatening cardiac arrhythmia.
- A QRS interval greater than 160 milliseconds increases the chance of ventricular arrhythmias to greater than 50%.
- Clinical pearl: A very wide complex ventricular rhythm, concomitant hypotension and/or seizure disorder is suspicious for toxic ingestion and standard ACLS algorithm will not suffice, treatment must address the underlying culprit (i.e. TCA --> Tx. fluids, vasopressors, sodium bicarbonate, and intravenous lipid emulsion).
Kerr GW, McGuffie AC, Wilkie S. Tricyclic antidepressant overdose: a review. Emerg Med J. Jul 2001;18(4):236-41.
Category: Cardiology
Keywords: Hypertrophic Cardiomyopathy (PubMed Search)
Posted: 8/3/2014 by Semhar Tewelde, MD
Click here to contact Semhar Tewelde, MD
Advances in Hypertrophic Cardiomyopathy (HCM)
- HCM is a genetically transmitted autosomal dominant disorder with two variants: hypertrophic obstructive cardiomyopathy (HOCM), also known as idiopathic hypertrophic subaortic stenosis (IHSS) or asymmetric septal hypertrophy, and non-obstructive hypertrophic cardiomyopathy (HNCM), also known as Yamaguchi syndrome.
- The most serious complication of both variants of HCM is sudden cardiac death (SCD) and end-stage heart failure, which rapidly progresses to cardiac death after its occurrence.
- Beta-blockers (1st line) and non-dihydropyridine calcium channel blockers are effective at improving clinical symptoms (syncope, dyspnea, chest pain, and exertional intolerance, etc.) however neither alone nor combined halt the progressive LV remodeling and prevent end-stage heart failure.
- Cardiac transplantation is the only treatment available for end-stage heart failure, but must occur before the onset of pulmonary hypertension, kidney malfunction, and thromboembolism for success.
- Class Ia anti-arrhythmic, disopyramide has been shown to be effective for symptomatic improvement (NYHA classification), but does not improve overall LV function or hypertrophy.
- A recent study found that another class Ia anti-arrhythmic, cibenzoline has been shown not only to reduce symptoms, but also improved LV diastolic dysfunction and induced a regression of LV hypertrophy. In this study cibenzoline has halted the progression of HCM to end-stage heart failure.
Hamada M, Ikeda S, et al. Advances in medical treatment of hypertrophic cardiomyopathy. Journal of Cardiology. July 2014 (64):1;1-10.
Category: Cardiology
Posted: 7/27/2014 by Semhar Tewelde, MD
(Updated: 11/21/2024)
Click here to contact Semhar Tewelde, MD
HIV & Atherosclerosis
Advances in antiretroviral treatment has increased the life expectancy of patients with HIV significantly, AIDS-related deaths have fallen by 30% since they peaked in 2005.
HIV infection predisposes to a chronic inflammatory and immunologic dysfunctional state, subsequent highly active antiretroviral treatment (HAART) results in metabolic changes and dyslipidemia.
In the post-HAART era, CAD is now considered to be the main cause of heart failure in HIV-infected patients, superseding the prior most common etiologies myocarditis and opportunistic infections.
The presentation of CAD in HIV-infected patients is largely similar to that in the general population with the exception is that they present at a younger age.
Certain antiretroviral agents specifically protease inhibitors have conventionally been associated with lipid dysfunction, further complicating the HIV-infected patients milieu.
Recent research has shown that a C-C chemokine receptor-type 5 (CCR5) antagonists has emerged as a potential target both as an antiretroviral agent as well as in the process of arresting atherogenesis, but warrants more research.
Ng B, MacPherson P, et al. Heart failure in HIV infection: focus on the role of atherosclerosis. Current Opinion in Cardiology. Issue: Volume 29(2) pgs. 174-179 March 2014.