Cardiology Newsletter Volume 7 No 1February 2016

Sponsored in the interests of continuing medical education by:

CPD Accredited

• Decision making in patients presenting with syncope• ESC 2015 Reportback• Medical Schemes Act – proposed changes to PMBs:

Implications for patients and health care providers

Page 3 Volume 7 No 1 February 2016

Editorial

Cigarette SmokingDr Mike Bennett

CardiologistWilgers Hospital, Pretoria

moking is the most preventable cause of death worldwide and millions around the world are se-riously ill due to diseases caused by smoking. In 1950 Hill and Doll first reported the association be-

tween lung cancer and tobacco, and in 1954 the mortality of doctors in relation to their smoking habits. Sixty-five years later we are still facing the same issues despite a wealth of information regarding the disastrous health risks associated with tobacco smoking. Russell wrote that “People smoke for the nicotine but they die from the tar”. Furthermore, it is dis-turbing that smoking not only affects the smoker but a large number of innocent bystanders (including children) exposed to second-hand smoke.

The first South African National Health and Nutrition Examination Survey (SAN-HANES-1) investigated the smoking status of South Africans and found that 17.6% of adults are smoking. Significant-ly more men than women are smokers (29.2% vs 7.3%). Among current smok-ers, more than 80% noticed the health warnings on the tobacco packages and approximately 50% considered quitting smoking but never did. Only 29.3% of current smokers were advised by health professionals to quit smoking – are we as doctors doing our job?

It is ironic that the tobacco plant, unlike humans, uses nicotine as a toxic substance to repel insects. Nicotine is similar in struc-ture to acetylcholine and binds to recep-tors in the brain resulting in dopamine release and activating the reward areas of the brain. This results in the satisfaction and reward associated with smoking.

Nicotine is an extremely addictive drug and has similar relapse rates to those of heroin with a 60% relapse rate after 3 months, and 80% after 12 months. Disap-pointingly, large numbers of smokers con-tinue to do so after a myocardial infarction and many women continue to smoke dur-ing pregnancy. In the SANHANES-1 survey subjects continued smoking despite read-ing the health warnings on the packages.

Several strategies have been tried to facil-itate smoking cessation with disappoint-ing results. Reduction of the nicotine con-tent of the standard-strength cigarettes (currently ~16 mg/gm tobacco) to a lower content (0.4 to 0.5 mg/mg tobacco) has been proposed as a means of reduc-ing tobacco dependence and to wean cur-rent smokers off cigarettes. In a recent trial regular smokers who switched to low-nicotine cigarettes for 6 weeks had reductions in nicotine exposure, num-bers of cigarettes smoked, and nicotine dependence.

Electronic cigarettes (e-cig) are battery-powered devices that aerosolise nicotine into a chemical propellant. Supporters of e-cig claim that not only are e-cig an effective harm reduction measure but also potentially superior to other smoking cessation products. E-cigs allegedly do not create the carcinogenic combustion products found in conventional paper cigarettes but propellants used in these devices decompose into known carcinogens. Reviewing 59 e-cig retail web sites, the most popular claims were that the products are healthier (95%), cheaper (93%), cleaner than cigarettes (95%), can be smoked anywhere (88%), and do not produce second-hand smoke (76%).

A recent study evaluated whether e-cig use among 14-year-old adolescents who have never tried combustible tobacco is associated with risk of use of combusti-ble tobacco products. Past 6-month use of any combustible tobacco products was more frequent in base-line e-cig ever users than never-users at the 6-month follow-up (30.7% vs 8.1%, respectively); and at the 12-month period follow-up (25.2% vs 9.3%, respectively). Further analysis revealed that adolescents who ever smoked were more likely to initiate e-cig smoking use during the follow-up period. It is not clear whether e-cig smok-ing leads to regular and frequent use of combustible tobacco.

Nicotine has potent addicting qualities and therefore people should be discour-aged from ever experimenting with it.

Adolescents and school children are par-ticularly vulnerable and parents should not only warn them about starting, but also explain to them the long-term con-sequences associated with tobacco use. The available evidence does not support many of the claims made by the e-cig in-dustry. E-cigs are safer than the conven-tional paper cigarettes and associated with fewer cigarettes smoked and there-for potentially cause less harm, but not safe enough to consider as an alternative to conventional cigarettes.

More than 50% of smokers continue to do so after a cardiovascular event and improved cessation aid is required. Psychosocial interventions (behavioral therapies, telephone support and self-help material) and the intensity and duration of such aid, have been shown to promote abstinence for up to a year. Surveys have shown that implement-ing smoke-free legislation covering bars restaurants and workplaces consistently reduced cigarette smoking. Home and work-place smoking bans lead to 65% higher likelihood of smoking cessation for people working or living in such plac-es. Smokers living in a smoke-free home were 70% more likely to quit than those in homes where smoking was allowed. Smoking cessation occurs in 58% of ex-smokers not exposed to passive smoking compared with ~25% of those exposed to passive smoking. Moreover, passive smoking increases the risk of coronary heart disease by 25-30% in non-smokers living with a smoking companion.

We, as parents and health workers, should go out of our way to spread the message about the deleterious long-term health consequences associated with the use of tobacco products. No smoker should be regarded as a lost case. To those of our colleagues who are still smoking, please think again about your health and also the message you are sending out to your patients. It is sad state of affairs when we need a “nanny state” to protect ourselves against the obvious.

References available on request.

Volume 7 No 1 February 2016 Page 4

ransient loss of conscious-ness (TLOC) is a term that encompasses all disorders characterised by transient, self-limited, non-traumatic

loss of consciousness. Syncope is differ-entiated from other forms of TLOC by its physiology (transient global cerebral hypoperfusion due to a sudden drop in peripheral resistance and/or cardiac output).

Patients may present with syncopal symptoms typical of a clinical condition but sometimes with vague symptoms of dizziness, giddiness, balance disturbances, presyncope or syncope. In most cases the clinician should be able to make a diagnosis by taking an accurate, detailed history and performing a physical examination.

The key to resolving the problem is to make sure exactly what the patient means and therefore finding out what happened is more important than believing that the patient’s choice of terms reflects what really happened during the event. Clinicians should therefore have a clear understanding of what the following terms mean:1. Syncope: transient loss of

consciousness (TLOC) due to transient global cerebral hypoperfusion with rapid onset, short duration and spontaneous complete recovery.

2. Presyncope: the sensation of impending loss of consciousness

3. Vertigo: the sensation of abnormal movement when no movement is occurring; usually the room spinning around the patient. It is not associated with any change of consciousness.

4. Dizziness: a sensation of disturbed spatial sensation, no change in consciousness and no awareness of any movement.

Pathophysiology of SyncopeSyncope is divided into 3 different groups according to the pathophysiology of the decreased global cerebral

hypoperfusion. Loss of consciousness (LOC) is known to result from:• sudden cessation of cerebral blood

flow (CBF) as short as 6-8 seconds; • a drop of systolic blood pressure

(SBP) of >60 mm Hg; • a combination of both. Systemic

BP is determined by cardiac output (CO) and total peripheral resistance (TPR) and a drop of either, usually a combination of both, can cause syncope.

An important determinant of CO is adequate cardiac stroke volume, which in turn is effected by heart rate (excessive tachy- or bradycardia) or a tachy- or bradyarrhytmia.

Common clinical syndromes

Reflex syncope (neurally mediated syncope) This is associated with malfunction of cardiovascular reflexes that normally help in maintaining the circulation. Vasodepressor syncope occurs when hypotension is the predominant problem (due to loss of upright vasoconstrictor tone) and cardioinhibitory syncope when bradycardia, or even asystole, predominates. A combination of the two mechanisms often occur.• Vasovagal syncope (VVS) is

mediated by emotion or orthostatic stress. It is frequently preceded by symptoms of autonomic activation like sweating, pallor and nausea and not by convulsion, tongue biting or loss of bladder control. In young people it usually follows a benign course and can be diagnosed from the history alone. Virtually all episodes of VVS are preceded by prodromal symptoms which start within 60 seconds before the loss of consciousness. Although fully awake and with no localising neurological signs, patients may feel dazed and exhausted after an event. In older people it is more likely due to a dysautonomic response representing an inability to adapt to physiological challenges resulting in

a progressive fall in heart rate and/or BP before the onset of symptoms. VVS has multiple triggers including a warm environment, prolonged standing, dehydration, alcohol and patients taking diuretics, anti-hypertensive and vasodilator medications

• Situational syncope is associated with some specific situations. Common situations include post-exercise syncope in athletes, cough and sneeze, post-micturition, post-prandial and gastrointestinal (swallow, defecation, visceral pain).

• Carotid sinus syncope is triggered by mechanical stimulation of the carotid sinuses resulting in a ventricular pause lasting >3 seconds and/or a fall in systolic BP. Clinical clues include triggers such as head turning, tight collars and shaving and is a condition of the elderly. Carotid sinus massage (CSM) should be performed in all patients over 40 years of age with unexplained syncope. CSM is contraindicated in patients with recent myocardial ischemia or carotid bruits unless significant stenosis has been excluded by carotid duplex-doppler.

Orthostatic hypotension (OH) OH is defined as an abnormal decrease in systolic BP upon standing. Although reflex syncope and OH have different pathophysiological mechanisms, the clinical manifestations of the two conditions overlap and could be confusing. Orthostatic intolerance refers to symptoms and signs in the upright position due to a circulatory abnormality and include syncope and pre-syncope, dizziness and lightheadedness, visual disturbances, palpitations and sweating. It is associated with standing up, or prolonged standing in crowded and/or hot environments.• Classical OH is defined as a decrease

in systolic >BP 20 mmHg and in diastolic BP >10 mmHg within 3 min of standing with accompanying symptoms. In the absence of

Dr Mike Bennett Cardiologist Wilgers Hospital, Pretoria

Decision making in patients presenting with syncope

Page 5 Volume 7 No 1 February 2016

symptoms, the above BP reductions cannot be ignored and should be considered positive if the presenting symptoms could be explained by orthostasis.

• Initial OH is characterised by BP decrease immediately on standing of >40 mm Hg with rapid (within 30 s) and spontaneous normalization of BP and symptoms.

• Delayed (progressive) OH is more common in the elderly and attributed to age-related impairment of compensatory reflexes and sensitivity to a decrease in venous return on standing. Delayed OH is characterised by a slow progressive decrease in systolic BP with a notable absence of a bradycardic reflex, which differentiates it from reflex syncope.

• Postural orthostatic tachycardia syndrome (POTS) occurs mostly in young women and presents with severe orthostatic intolerance, but not syncope, with a very marked HR increase (>30 bpm or to >120 BPM) and instability of BP. POTS is frequently associated with chronic fatigue syndrome.

• Medication-Induced orthostatic hypotension should always be considered in the elderly. Frequent culprits include: α-blockers, diuretics, nitrates, neurological medications, anti-parkinsonian, anti-depressants and benzodiazepines.

Cardiac syncopeCardiac syncope is characterised by no warning symptoms of dizziness, light headedness or nausea with injuries to the patient on his way down. Depending on the duration and severity of the cerebral hypoperfusion, convulsions may occur and may clinically be impossible to discriminate from seizures. Studies using implantable loop recorders have found cardiac arrhythmias to be the cause of seizure symptoms in a large number of patients with an epilepsy diagnosis, who were treatment-resistant or had atypical seizures,

• Bradycardia due to a brady-arrhythmia, atrioventricular conduction disease or drugs (beta blockers, calcium channel blockers).

• Tachy-arrhythmias (atrial, ventricular, pre-excitation, congenital or acquired Long-QT syndromes) may present with syncope or near-syncope before vascular compensation develops. As soon as vascular compensation kicks in, consciousness is restored even before the arrhythmia terminates. If vascular compensation is inadequate, consciousness may not recover spontaneously, and the event may present as a cardiac arrest.

• Structural heart disease including valvular disease, cardiomyopathies, coronary artery disease, pulmonary hypertension, pulmonary embolism.

• Cardiovascular Drugs. Several commonly used CV drugs may cause hypotension, excessive bradycardia, A-V block and may be pro-arrhythmogenic.

Exercise and SyncopeSyncope related to exercise, may or may not be related to underlying cardiovascular disease. Again the history of the event is of paramount importance. Syncope that occurs after exercise or during breaks, is unlikely to be life-threatening, and likely related to vasodilatation with corresponding hypotension. Syncope during exertion

is more likely to be life-threatening especially if there were no warning symptoms. The underlying heart problem in the older population is often of ischemic origin, and in the younger population hypertrophic cardiomyopathy, coronary artery anomalies, arrhytmogenic right ventricular dysplasia, pre-excitation or other genetic diseases should be excluded. A family history of early sudden cardiac death may point to an inherited life-threatening heart condition.

Syncope during exertion of sudden onset without any warning symptoms resulting in injuries requires a full cardiac evaluation.

Which investigations should be considered?History taking. It is important to realize that the cornerstone of a proper assessment is good history taking. The elderly may not be able to recall what exactly happened and the accounts of witnesses are extremely helpful.

Vital historical features that must be considered include:1. Position or change of position that

preceded the syncopal attack.2. Activity preceding the attack (aortic

valve stenosis, pulmonary hyper-tension, obstructive cardiomyo-pathy, coronary artery disease).

3. Prodromata4. Cardiac related symptoms like chest

pain or palpitations.5. Duration of the event6. A pale and clammy appearance

before and during the event suggests hypotension

7. Abnormal movements: jerking of the body may be due to a seizure, but brief clonic activity may occur with syncope due to hypotension

8. Medical history of cardiac (heart failure, coronary artery disease or neurological disease (migraine, Parkinsonism, epilepsy)

9. Medication, especially in the older patient.

The key to resolving the problem is to make

sure exactly what the patient means and

therefore finding out what happened is more

important than believing that the patient’s choice

of terms reflects what really happened during

the event.

Volume 7 No 1 February 2016 Page 6

10. Family history of sudden death, especially in the younger patient population.

The clinical examination should include heart rate and rhythm, BP, and a focused cardiac and neurological examination. Heart murmurs and carotid bruit should be investigated.

Rule out orthostatic hypotension and do carotid sinus massage where indicated.

Electrocardiogram is mandatory and should be recorded as soon as possible, especially when an arrhythmia is present. Any recordings by emergency personnel must be scrutinised for rate and rhythm abnormalities. An ECG recording while the patient is symptomatic is invaluable and if normal, excludes a cardiac cause for the syncope. Bundle branch block associated with atrio-ventricular (A-V) conduction abnormalities is suggestive of an intermittent A-V block. Exclude causes like pre-excitation, long QT-syndromes, Brugada syndrome on the 12-lead ECG, left ventricular hypertrophy or evidence of myocardial ischemia.

Exercise testing (ET) is of value when the patient’s symptoms are associated with physical exertion and routine ET in patients with syncope is not recommended. It must be considered in patients with previous coronary artery disease or existing heart disease.

Holter monitoring is of limited use unless the events occur frequently (almost daily). The commonly used systems monitor a patient for only 24-48 hours. Symptoms occurring in the absence of arrhythmias or conduction abnormalities, exclude a rhythm disturbance as a cause of syncope. A common problem is what to make of arrhythmias recorded that are not accompanied by the patient’s presenting symptoms. Normal ambulatory ECG in the absence of symptoms does not exclude a causal arrhythmia or conduction abnormality and monitoring for longer periods are necessary.

Tilt-table testing is a useful tool to demonstrate a patient’s susceptibility to reflex syncope. It is not indicated with typical reflex syncope.

Loop recorders are expensive and invasive but allow for an extended period of monitoring and are extremely reliable to lead to confirmation or exclude a cardiac etiology as the cause of the event. Loop recording should be considered in all patients in whom the symptoms are associated with injuries or the patient’s occupation put him or others at risk. They are particularly effective in older patients (diagnostic rates of up to 50%) in view of the disproportionately high number of cardiac causes in this population presenting with syncope and unexplained falls.

Echocardiography should be reserved for patients with a clinical indication. Patients with a heart murmur (especially aortic valve stenosis in the elderly) and heart failure (determine ejection fraction) since cardiac arrhythmias are present in up to 50% of an EF <40%.

Ambulatory blood pressure monitoring may be useful in recognising postprandial hypotension, hypotension after medication ingestion, orthostatic and exercise-induced hypotension.

EEG should not routinely be requested unless clinical clues indicate a reasonable likelihood of a neurological cause.

Carotid artery duplex-Doppler not routinely indicated unless neurological signs and symptoms indicate a reasonable likelihood.

Brain imaging must be requested by a specialist and is not routinely recommended.

ConclusionSyncope is one of the most common clinical events in medicine. The physician’s fear of missing a serious condition with the associated negative consequences may lead to tests and treatments that are inappropriate. High-risk patients are those that may have a fatal cause of syncope and specific risk markers exist which help to identify those patients. Until a diagnosis is made, no appropriate treatment can be instituted. A thorough question-and-answer consultation covering every detail of the patient’s presentation is required.

References1. Moya A, Sutton R Ammirati F, et al.

Guidelines for the diagnosis and management of syncope (version 2009). Eur Heart J 2009;30:2631-71

Table 1. Short-Term High-Risk Criteria that require Prompt Hospitalization or Early Intensive Evaluation.

Severe structural or coronary artery disease (heart failure, low ejection fraction, or previous myocardial infarction).

ECG features suggesting arrhythmic syncope (nonsustained ventricular tachycardia, bifascicular block, sinus bradycardia, sinoatrial block, pre-excitation, prolonged QTC

Clinical features suggesting arrhytmogenic syncope (syncope during exertion or supine position, palpitations at the time of syncope, family history of sudden cardiac death).

Important comorbidities ( severe anemia, electrolyte disturbance)

Page 7 Volume 7 No 1 February 2016

Dr Mike Bennett Cardiologist Wilgers Hospital, Pretoria

Congress ReportbackEuropean Society of Cardiology Congress 2015

he recent ESC meeting held in London, UK did not disap-point. The only possible dis-appointment might have been the number of presen-

tations that one could not attend be-cause of overlapping sessions. It is im-possible to give an overview of the whole meeting and this report is a sum-mary of the most interesting sessions I attended. I chose topics that were of clinical interest to me and expect to be-come part of our clinical practice in fu-ture.

Heart Failure (HF)We all await the new HF drug, valsartan-sacubtril (Angiotensin receptor/neprilysin inhibitor= ARNI), which has already been approved in Europe. This drug is a combination of valsartan and a drug that inhibits the degradation of vasoactive peptides (pro-BNP). Previous studies have confirmed the benefits of this drug on mortality, morbidity, and reduction in hospitalisation and reduction in side effects. The Paradigm HF showed at a mean follow-up of 27 months in comparison to enalapril, ARNI reduced the risk of death by 16%, cardiovascular death by 20%, and hospitalisation by 21% (NEJM 2014;371:993-1004). Hypotension and non-serious angioedema occurred more frequently in the treatment group but with less renal impairment, hyperkalemia and cough.

It was proposed that ARNI be considered as first line treatment in patients with HF and reduced ejection fraction. This drug is not currently available in RSA.

Although mineralocorticoid receptor antagonists (MRAs) have demonstrat-ed reduced mortality in myocardial in-farction (MI) patients with HF, spironol-actone 25 mg/d for 6 months in post-MI survivors without HF, did not result in the reduction of death, resuscitated death, VF/VT or HF. There is therefore no evidence supporting the routine use of spironolactone post MI in patients without HF.

DigitalesThe role of digoxin in patients with systolic heart failure (HF) is controversial. Newer treatment strategies (ACE-I/ARB, Beta-Blockers, MRA’s) are the first-line drugs for patients with systolic HF and the role of digoxin on top of these drugs is not clear. A Danish study assessed the safety and effectiveness of digoxin-treated patients vs no digoxin in 21,665 patients with atrial fibrillation (AF) and HF over a period of 5years. The rate of readmission for heart failure was similar between the two groups and not influenced by the severity of the HF. The all-cause mortality was slightly lower (5.4 vs 5.8 deaths per100 person-years) in the digoxin-treated patients and was lowest in patients with more severe HF. It is some good news for those of us who still use digitales in patients with symptomatic HF and AF already on optimal medical therapy.

Hypertension1. In the PARAMETER study ARNI

was compared to olmesartan in ~450 elderly patients (median age 68 years). After 12 weeks the ARNI-treated patients showed a systolic blood pressure (SBP) reduction of 12.6 mmHg versus 8.9 mmHg in the olmesartan group (p=0.01). Central aortic pressure was reduced by 6.4 mmHg in the ARNI group compared to 4.0 in the olmesartan group. The 24-hour ambulatory monitoring was reduced by an additional 4.1 mmHg and central SBP by an additional 3.3 mmHg (p<0.001). Almost 50% of olmesartan patients required add-on medication compared to 32% in the ARNI group. The ARNI group had 34% reduction in baseline NT-pro BNP compared to 20% for olmesartan. Changes in arterial distensibility are thought to be the mechanism of the drug.

2. Resistant hypertension The PATHWAY-2 studied 335 pa-tients with resistant hyperten-sion already treated according to guidelines (ACEI/ARB+ Ca-channel blocker + thiazide-like diuretic). Pa-tients were randomised to 12 weeks of spironolactone (25-50 mg), biso-prolol (5-10 mg), doxazosin (4-8) mg, and placebo. Spironolactone reduced home SBP by 8.7 mmHg compared to placebo (p<0.001) and 4.26 mmHg more than bisoprolol/doxazosin (p<0.001). Spironolac-tone controlled 60% of previously uncontrolled patients and was 3 times more likely than bisoprolol or doxazosin to exert control. It may be necessary to reconsider treat-ment algorithms considering the efficacy of such a cheap drug in this very high-risk group of patients.

The value of a midday napA study from Greece reported the benefit of taking a midday nap (siesta) in 386 middle-aged hypertensive patients whose midday sleep time, pulse wave

Congress highlights of the ESC 2015 Congress, held

on the 29th August - 2nd September 2015

in London.

Volume 7 No 1 February 2016 Page 8

velocity, lifestyle habits, BMI and left atrial size were measured. Midday sleepers have a 5% lower average 24-hour ambulatory systolic BP (6 mmHg) than those not taking their siesta. The longer the midday sleeps, the lower the systolic BP levels.

PacingThe result of a new leadless cardiac pacemaker system that is percutaneously inserted was reported. The device is a fully self-contained, leadless pacemaker with combined battery, electronics, and electrodes in a small unit that is implanted directly in the right ventricle with the use of a catheter through the femoral vein. After 6 months 93.4% of patients reached the primary efficacy endpoint (a pacing threshold of <2.0 v at 0.4 msec and a sensing amplitude of >5.0 mV) in 90% of 526 patients.

Complications included cardiac perforation (1.3%), device dislodgement (1.7%), elevated thresholds necessitating device retrieval (1.3%) and vascular complications (1.3%). Devices were retrieved up to a year but it is unknown whether this will be possible after many years or whether the device will simply be abandoned.

The investigators estimated battery longevity to be 15 years. Advantages of the leadless system include avoidance of the surgical pocket with bleeding, infection, venous occlusion, pneumothorax, lead-related failure and tricuspid valve regurgitation. It will only be considered for patients requiring a single-chamber pacemaker.

Coronary artery disease1. Reducing myocardial infarct

size In a previous proof-of-concept trial the same authors found that cyclosporine reduced myocardial infarct size in patients with STEMI. In a follow-up trial including 970 patients with an acute anterior myocardial infarction undergoing

percutaneous coronary interven-tion, received intravenous cyclo-sporine or placebo before coronary recanalisation. Disappointingly, cyclosporine did not reduce the clinical components of the prima-ry outcomes (death of any cause, worsening of heart failure during the initial hospitalisation, rehospi-talisation). This trial underscores the fact that good theoretical rea-soning does not necessarily trans-late into clinical benefit.

2. Role of Vulnerable plaque Patients who suffered a MI have an estimated risk of 10% of a coronary event during the following year and a 5% in each of the subsequent years. Studies have shown that patients with a previous MI are very likely to have other vulnerable plaques, placing them high risk for future events.

A vulnerable plaque has a high risk of disruption leading to thrombosis. Autopsy studies have shown that in 55-60% of subjects had plaque rupture, 30-35% had erosion, and 2-7% had thrombi attributed to calcified nodules. The most typical plaque prone to rupture is the thin-cap fibroatheroma (TCFA) characterised by a thin overlying cap and large necrotic core.

It is important to realize that not all TCFA will rupture and not all ruptures will present as an acute coronary syndrome. Unfortunately, evaluating potential vulnerable plaque requires an invasive procedure and includes imaging technologies like intravascular ultrasound (measures vascular lumen and plaque volumes), optical coherence tomography (ideal for measuring the fibrous cap thickness) and near infrared spectroscopy (assesses cholesterol within lipid and necrotic cores).

The optimal treatment to prevent rupture or erosion of vulnerable plaque is yet to be determined but aggressive control of known risk factors goes a long way.

3. Guidelines for non-STEMI acute coronary syndrome (ACS) The incidence of STEMI has decreased appreciably over the past decade, and more patients with unstable angina were reclassified as having NSTEMI utilising more sensitive biomarkers. High-sensitive cardiac troponin (hsTrop) allows reliable detection of lower serum troponin levels resulting in a higher negative predicting value and reducing the “troponin-blind” interval leading to earlier detection of ACS.

Current guidelines recommend de-termination of Trop on presentation and repeat after 3 hours if the initial value is within normal limits.

In the Biomarkers in Acute Cardio-vascular Care (BAAC) hsTrop I af-ter 1 hour was compared to stand-ard 3-hour strategy and it was determined that the best hsTrop I value to rule out AMI was 6 ng/L.

In >75,000 individuals from the general population, hsTrop I lev-els >6 ng/L predicted an increased risk of death or cardiovascular

A vulnerable plaque has a high risk of disruption

leading to thrombosis. Autopsy studies have

shown that in 55-60% of subjects had plaque

rupture, 30-35% had erosion, and 2-7% had

thrombi attributed to calcified nodules.

Page 9 Volume 7 No 1 February 2016

disease (BIOmarCaRE) suggesting that even slightly elevated Trop I levels are important predictors of cardiovascular disease.

Applying the new cut-offs to the BAAC population, that mortality would have been lower if patients had been triaged with the 1-hour algorithm compared to the routine 3-hour approach. The shorter al-gorithm had a 99.7% negative pre-dictive value.

The final conclusion is that using more sensitive cut-offs all patients at risk can be identified and low risk patients may be identified earlier and more accurately.

4. Dual antiplatelet therapy (aspirin combined with P2Y12 inhibitor) is indicated in all patients presenting with ACS. Prasugrel and ticagrelor are preferred over clopidogrel be-cause of improved ischemic out-comes. Preloading with prasugrel prior to coronary angiography in NSTEMI-ACS is discouraged based on increased bleeding risk in the ACCOAST trial.

5. Glycoprotein IIb/IIIa inhibitors should only be used as bail-out for periprocedural complications.

6. High-dose statins should be initiated as soon as possible and maintained long-term.

7. Coronary angiography (CA)The importance of invasive angiogra-phy with intention to revascularisa-tion is recommended as the preferred approach. Immediate angiography is recommended for high-risk patients (shock, continuing chest pain, cardiac arrest, life-threatening arrhythmias) and CA within 24 hours of presenta-tion in the absence of the above but with diagnostic troponin changes, dynamic ST- or T-wave changes and/or a GRACE score of >140.

8. In patients with diabetes mellitus or multivessel disease and acceptable surgical risk, coronary artery bypass grafting is recommended over percutaneous coronary intervention.

9. Risk of air pollutionAir pollution is now ranked ninth among the greatest modifiable risk factors for cardio-vascular disease. It is important to realise that air pollution not only exacerbates existing heart conditions but also plays part in their causation. The main culprit is fine nanoparticles (Particulate matter <2.5 μm = PM2.5) which appear in diesel and petrol exhaust fumes and are small enough to enter deep into the lungs and may reach the bloodstream.

A study, involving >65,000 women, showed an increased risk of 1.76 for death from CVD for every10 g/3 in mean concentrations of PM2.5. Previous studies have shown that diesel exhaust fumes exacerbated exercise-induced ischemia and impaired endogenous fibrinolysis in men with CAD.

The effect of air pollution on cardiovascular risk in young adults (age 16-22 years) was investigated in a study from Poland. A group of young adults with similar

social backgrounds was selected from two cities with different air pollution levels. Average air pollution levels (PM2.5 and PM10) were nearly doubles that of the other city.

The investigators found significantly higher levels of CRP, hsCRP, homocysteine and fibrinogen in the subjects from the worst polluted city. The highest levels of these inflammatory markers were found in overweight patients from the most polluted city.

The investigators concluded that living in a highly polluted city have an impact on cardiovascular markers even at an early age.

These findings have serious implications for people living in severely polluted areas and authorities should once again take cognisance of the wide ranging health risks air pollution poses to the inhabitants of those cities. The public and authorities are not sufficiently aware of the substantial impact that air pollution is having on CVD.

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Air pollution is now ranked ninth among

the greatest modifiable risk factors for cardio-

vascular disease. It is important to realise that

air pollution not only exacerbates existing heart

conditions but also plays part in their causation.

Volume 7 No 1 February 2016 Page 10

Ms Elsabe Klinck B.Iur (UFS) LL.B (UFS) BA Hons (German) (UFS) BA Applied Psychology for professional contexts (Unisa)EK Consulting

Medical Schemes Act – proposed changes to PMBs: Implications for patients and health care providers

n July this year, the Minister of Health published proposed amend-ments to the Prescribed Minimum Benefit (PMB) Regulations for comment (Government Gazette No

38990 of 14 July 2015). The comment period closed in October 2015. The pro-posal has been seen by many as a threat to private practice. In this article we will unpack what the proposed changes en-tail, and what that could mean for pro-viders and patients, if adopted.

The PMBs in law and practiceThe PMBs are benefits that all medical schemes, on all options, should fund. It is a key element of what makes medical scheme cover “social insurance” as opposed to regular insurance. Under the PMBs, one obtains cover for one’s health condition, irrespective of how healthy, ill or old one is. In regular insurance, one is penalised for one’s health status, age, etc., i.e. the risk one poses. PMBs are therefore “social security” benefits. They aim to give everyone some core of benefits, so as to prevent persons from falling through the cracks on important conditions, or from having to utilise the public sector when they have run out of funds. People are, therefore, through a mechanism of shared (“social”) pooling of funds, covered or insured.

There are 270 diagnostic and treatment pairs that make up the PMBs, and 25 chronic diseases which all fall within the “must be funded in full” category. All emergency care is also included in this.

Because a scheme has to fund the PMBs, and has to cover it for low-, or no-, and high risk patients, the complaint that the PMBs are “too expensive” is often heard. The 2015 Council for Medical Schemes Annual Report sets the costs of the PMBs as follows:

• It costs, on average, R552.30 per beneficiary per month to provide the full set of PMBs;

• PMB costs amount to 52% of the total scheme risk pool, i.e. 48% of spend goes towards non-PMB conditions

• Of all the benefits paid by schemes, PMBs constitute 46% of expenditure.

There are therefore significant portions of medical scheme expenditure that

are discretionary to the scheme, and it appears strange that one would aim to erode the core of what is mandated, and increase the proportion of non-core, scheme discretionary spend. This would go against the constitutional imperative in the South African Bill of Rights, i.e. that everyone is entitled to access social security.

The PMB proposal

Limiting the reimbursement levelThe July 2015-proposal aims to limit the exposure of schemes to the PMBs, by capping what would have to be covered for professional fees of healthcare professionals, to treat the PMBs, at pre-determined levels. This means that schemes would still have to cover a PMB, but only up to a certain level.

It is proposed that that level be set at the 2006 NHRPL, adjusted by inflation. The 2006 National Health Reference Price List (NHRPL) was the last list published by the Council for Medical Schemes prior to the implementation of the Reference Price List (RPL) by the National Department of Health, in terms of the National Health Act. The RPL constituted a reference list, and both providers and schemes were still free to set their prices and reimbursement levels as they deemed proper and reasonable, but with reference to the RPL.

The proposed amended regulation is worded as follows (underlined):

(2) …, the rules of a medical scheme may, in respect of any benefit option, provide that—(a) the diagnosis, treatment and care

costs of a prescribed minimum benefit condition will only be paid in full by the medical scheme if those services are obtained from a designated service provider in respect of that condition;

(b) a co-payment or deductible, the quantum of which is specified in the rules of the medical scheme, may be imposed on a member if that member or his or her dependant obtains such services from a provider other than a designated service provider, provided that no co-payment or deductible is payable by a member if the service was involuntarily obtained from a provider other than a designated service provider; and either

(i) in respect of any service rendered by a health care professional who is registered with the Health Professions Council of South Africa, medical schemes are liable for payment for services in accordance with the billing rules and the tariff codes of the 2006 NHRPL tariffs published by the Council, the Rand value of which has been adiusted annually in accordance with the Consumer

The July 2015 proposal aims to limit the exposure

of schemes to the PMBs, by capping what would

have to be covered for professional fees of

healthcare professionals, to treat the PMBs, at pre-

determined levels.

Page 11 Volume 7 No 1 February 2016

Price Index as published by Statistics South Africa; or

(ii) schemes may negotiate alternative tariffs with any provider of any relevant health service for which no co-payment or deductible is payable by a member.

What the proposal, if implemented, would mean is that, if, for example, a scheme received an account for a consultation with a patient with heart failure, which is a PMB condition, and the scheme has not entered into a designated service provider (DSP) agreement, the scheme would only have to fund the consultation up to the 2006-Rand values for a consultation, adjusted for inflation over the nine years till 2015.

Where the actual fees charged in 2015 differ from that schemes will have to pay, it will mean a co-payment to the patient or, for the practitioner, a lower level of fee. From a patient perspective it means that benefits levels which might have been set at amounts greater than what the 2006-adjusted price yield, have been effectively reduced. In effect, the draft proposals would amount to a statutorily-sanctioned reduction on fee and benefit levels.

The 2006 NHRPL Codes are outdatedA concern of stakeholders is that the 2006 NHRLP reflects the status of medical science at that time, which is more than 9 years ago. Recent developments in health technology, including procedure, hire fee and equipment use codes are not reflected in the 2006 NHRPL code. Neither are new ways of approaching treatment, which could affect the relativities between two professional actions, i.e. two codes that reflect those professional acts. It may now be possible to do things faster, or differently, or totally differently (e.g. things that could only be treated with medical devices can now be treated with medicine, or vica versa).

Is consumer price inflation (CPI) an appropriate measure?It is a well-known fact that medical inflation outstrips general inflation. Practitioners have also, in their various submissions to the Competition Inquiry into Private Healthcare, made the point that the cost of running a healthcare practice in general, and specific costs such as those relating to malpractice cover, have increased significantly.

Medical scheme premiums have, since 2006, increased above inflation, and therefore, to “set back the clock” for healthcare professional fees to fees far lower than scheme premium increases, appear not to make sense.

Table 1 from the Council for Medical Schemes (CMS)’s submission to the Competition Inquiry show the percentage points difference between premium increases and inflation.

Impact on DSPs or alternative tariff agreementsThe proposal does create an exception, i.e. when a scheme has entered into an agreement to provide preferential tariffs, they could do so. It is not clear from the proposed amendment how that would relate to the DSP

agreement provisions already in place in regulation 8(3). If, however, as is generally asserted, the statutory level (i.e. the 2006-adjusted levels) would be below the current reimbursement levels, schemes have no incentive to enter into “alternative tariffs” or DSPs. The end-effect is likely to be increased levels of co-payments and gap cover insurance.

Only healthcare professionals?It is also noteworthy that the proposal only limits its operation to healthcare professionals registered at the Health Professions Council of SA (HPCSA). Excluded from this reimbursement limitation are therefore hospitals and all healthcare professionals registered at other statutory bodies, such as nursing professionals, pharmacists and allied healthcare professionals (e.g. chiropractors).

The rationale for capping HPCSA-registered professional fees, but not that of hospitals, neither those applicable to other professionals, is not clear. The largest expenditure item of medical schemes, according to the CMS Annual Report of 2015, is hospitals, of which, in turn, the highest proportion relates to ward fees. Furthermore, the

Table 1. Overview of contribution increase trend (2001-2013)Year CPI Average Contribution Increase2001 6.6% 15.3 %2002 9.3 % 14.1 %2003 6.8 % 11.5 %2004 4.3 % 6.8 %2005 3.9 % 6 %2006 4.6 % 6.7 %2007 6.7 % 8.3 %2008 8.5 % 11.3 %2009 7.1 % 13 %2010 4.3 % 9.2 %2011 5.0 % 8.8 %2012 5.6 % 9.7 %2013 6.0 % 8.9 %

Source: CMS annual report (2001-2013)

Volume 7 No 1 February 2016 Page 12

CMS Annual Report makes it clear that expenditure associated with General Practitioners have stagnated, i.e. schemes are not spending more on GP costs at all.

Discharge ReportFurther amendments are also proposed to regulation 5. Regulation 5 sets the criteria for any healthcare account to be valid and acceptable to medical schemes. It now proposes the following to be added, and therefore to be made a pre-condition to payment of hospital accounts (proposed amendment underlined):

5. Accounts by suppliers of services.—The account or statement contemplated in section 59 (1) of the Act must contain the following—(a) The surname and initials of the

member;(b) the surname, first name and other

initials, if any, of the patient;(c) the name of the medical scheme

concerned;(d) the membership number of the

member;(e) the practice code number, group

practice number and individual provider registration number issued by the registering authorities for providers, if applicable, of the supplier of service and, in the case of a group practice, the name of the practitioner who provided the service;

(f) the relevant diagnostic and such other item code numbers that relate to such relevant health service;

(g) the date on which each relevant health service was rendered;

(h) the nature and cost of each relevant health service rendered, including the supply of medicine to the member concerned or to a dependant of that member; and the name, quantity and dosage of and net amount payable by the member in respect of the medicine;

(i) where a pharmacist supplies medicine according to a prescription to a member or to a dependant of a member of a medical scheme, a copy of the original prescription or a

certified copy of such prescription, if the scheme requires it;

(j) where mention is made in such account or statement of the use of a theatre—(i) the name and relevant practice

number and provider number contemplated in paragraph (e) of the medical practitioner or dentist who performed the operation;

(ii) the name or names and the relevant practice number and provider number contemplated in paragraph (e) of every medical practitioner or dentist who assisted in the performance of the operation; and

(iii) all procedures carried out together with the relevant item code number contemplated in paragraph (f); and…

(2) In the case of an account or statement of a hospital, the account or statement must be accompanied by a discharge summary prepared and provided by the attending healthcare provider. Such a discharge summary must contain adequate information to substantiate the diagnostic codes and other item code numbers specified in that account for the purposes of subregulation (1)(f).

It is unclear who this attending healthcare provider would be, and why the hospital account would be made subject to this summary report. The National Health Act, 2003 does envisage discharge reports to be provided, but the regulations pertaining to this topic to be made by the Minister of Health, are still outstanding. Section 10 reads as follows:

10. Discharge reports.—(1) A health care provider must provide a user with a discharge report at the time of the discharge of the user from a health establishment containing such information as may be prescribed.(2) In prescribing the information contemplated in subsection (1), the Minister must have regard to—

(a) the nature of the health service rendered;

(b) the prognosis for the user; and(c) the need for follow-up treatment.

(3) A discharge report provided to a user may be verbal in the case of an outpatient, but must be in writing in the case of an inpatient.

It is therefore not clear exactly what the content of the discharge report under the amended regulation 5 to the Medical Schemes Act is to entail, and who would take legal responsibility for its compliance. There is also no clarity on who will reimburse the practitioner for the time spent on completing this report, as it seems to not relate to the provider account for services, but rather the hospital account for services.

ConclusionMany stakeholders have commented on the draft amendments to Regulations 5 and 8 to the Medical schemes Act, 1998. It is argued that the amendments are not timed well, as proposals and recommendations in relation to the PMBs are bound to be made by the Competition inquiry Panel, which is currently investigating issues relating to cost, competition and fees in the health sector.

The absence of a PMB Review, which should, by law, take place every two years, has also exacerbated the PMB situation, as the PMB definitions have not been updated to consider developments since its initial promulgation.

The amendments appear to be part of a piece-meal approach to private health sector reforms, which are bound to have unintended consequences, the most obvious which will be, in this case, increased co-payments and the increased utilisation of gap cover. This goes against the clear policy objectives of both the CMS and the Department of Health.

Page 13 Volume 7 No 1 February 2016

Commentary on Current Journal Articles

Dukes DW, Dewland TA, Vittinghoff E, et al.

Study questionDoes the frequency of premature ventricular contractions (PVC) predict a decrease in left ventricular function (LVEF), incident congestive heart failure and death in a population- based cohort?

MethodsIn a prospective multicenter study 1,429 subjects 65 years or older who had normal LVEF and no prevalent CHF, were then followed with annual clinic and semi-annual telephone contact for 10 years, with 6-monthly telephone contact thereafter. All patients had 24-h ambulatory monitoring during their initial assessment and all PVC, atrial fibrillation (AF), and ventricular tachycardia (VT) episodes were identified.

Results1. Echocardiographic changes: over 5 years, each doubling

of the baseline PVC percentage was associated with a statistically decrease in the LVEF. Similar associations were observed when PVC percentages were analyzed as quartiles.

2. Incident CHF. Over a median follow-up of 13.7 years, 27% subjects developed CHF. PVC percentage and PVC percentage analysed as quartiles were associated with CHF. PVC were associated with systolic dysfunction but did not predict HF with preserved systolic dysfunction.

3. Mortality. Whether analysed as a continuous variable or as Quartiles, a higher PVC percentage was associated with an increased mortality.

4. Test characteristics. Using PVC percentages alone, the risk for CHF rose as the percentage of PVCs increased between 0% and 0.5%, with tapering of the risk curve for percentages >10%. The positive predictive value for the 15-year risk for incident CHF was >50% for PVC percentages between 1.24% and 3.55%

5. Population attributable risk. The risk of incident CHF that could be attributed to PVCs was 8.1% compared to

a reference population with PVC percentage equal to the lower quartile of the cohort (a similar magnitude to the risk of CHF that could be attributed to BMI, hypertension, age, and CAD).

ConclusionIn a population-based sample of subjects 65 years or older who were free of prevalent heart disease and normal LVEF, a higher frequency of PVCs was associated with a decrease in LVEF, an increase in incident CHF, and an increase in mortality

PerspectiveThe management of patients with PVCs and no evidence of structural heart disease is controversial. PVCs in patients without underlying heart disease have traditionally been regarded as benign but a PVC burden of as low as 10% has been recognized to lead to progressive LV dysfunction.

The exact mechanism is still unclear. Moreover, not all patients with frequent PVCs will progress to a CMP. The authors correctly point out that it is unclear whether PVCs are the presenting symptoms of an occult cardiomyopathy or whether they are the culprits causing CHF. Ablation of unifocal PVCs is an effective treatment modality in symptomatic patients but there is no evidence supporting ablation as a prophylactic treatment strategy to prevent incident CHF.

More information is required to identify asymptomatic patients who will benefit from a prophylactic and invasive procedure to prevent future heart disease. What this study highlights is that the increased risk of incident CHF and mortality is already present at a much lower PVC frequency even in healthy subjects.

By JM Bennett

Ventricular Ectopy as a Predictor of Heart Failure and Death

CPD AccreditationDoctors can acquire CPD points with this newsletter by visiting www.mpconsulting.co.za and completing an online MCQ consisting of 15 questions. Should you have any queries regarding the completion of the online MCQ, please contact:Inge Erasmus at 0861 111 335 or email: inge@mpconsulting.co.za.

Volume 7 No 1 February 2016 Page 14

Congress Reportback:

European Society of Cardiology Congress

Congress Calendar 2016Event/

Congress Date Venue Contact

Interventional Cardiology 31st Annual International Symposium 2016 (IC 2016)

6-11 March 2016

The Westin Snowmass Snowmass

Village, United States

http://promedicacme.com/meeting/Interventional-

Cardiology-2016-31st-Annual-111.

html

Africa PCR 2016

31 March

- 2 April 2016

Johannesburg, South Africa

www.africapcr.com/

info@eoafrica.co.za

American College Of Cardiology 65th Annual Scientific Session & Expo 2016 (ACC 2016)

2-4 April 2016

McCormick Place

Chicago, United States

www.expo.acc.org/ACC16/

Public/Enter.aspx

International Conference on Emergency Medicine and Symposia (ICEM)

18-21 April 2016

Cape Town International Convention

Centre, Cape Town, South

Africa

www.icem2016.org/

World Congress of Cardiology & Cardiovascular Health 2016

4-7 June 2016

Mexico City, Mexico

www.world-heart-federation.org/

wcc-2016