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ESC 2014 Feedback

Posted on Thursday, 25 September 2014 13:49

SA Heart had its own booth at the recent ESC congress. Read the feedback report from Dr Tony Dalby on the ESC content and highlights and SA Heart activities during the congress.

 

SA Heart had its own booth at the recent ESC congress and made good use of it.

Prof Johan Moolman (middle, now Australia, previously Tygerberg Hospital) catching up with Drs Naomi Rapeport and Colin Schamroth at the SA Heart booth during ESC congress

 

Also read the feedback report from Dr Tony Dalby on the ESC content and highlights

 

Prof Bongani Mayosi using the SA Heart booth as remote office during the ESC congress


Attachments:

Photo0237_480_360_80_s.jpg 31.7K 16 Apr 15 13:49
Photo0259_480_360_80_s.jpg 27.0K 16 Apr 15 13:49
ESC_2014_Report.pdf 290.1K 16 Apr 15 13:49
ESC_2014_Abbreviations.pdf 79.3K 16 Apr 15 13:49
SA_Heart_at_ESC_Congress_in_Barcelona.pdf 482.7K 16 Apr 15 13:49

Dr Makoali Makotoko has been appointed HOD at UFS

Posted on Wednesday, 27 August 2014 13:52

We congratulate Dr Makoali Makotoko who has been appointed head of department of cardiology at the University of the Free State. Dr Makotoko will take up the positin in January 2015.

We wish Dr Makotoko well and trust that her appointment will usher in a period of stability and a resumption of full cardiology service delivery to the people of the Free State.

Cardio update workshop for non-cardiologists at SA Heart Congress 2014

Posted on Thursday, 14 August 2014 13:56

After a decade, the 2014 SA Heart Congress has returned to Durban, where it will be hosting its annual cardio update for non-cardiologists on Thursday, 16th October, 2014 at the International Convention Centre.

Held in association with The Heart Failure Society of South Africa (HeFSSA), this comprehensive, pre-congress workshop targets primarily physicians and general practitioners, and is free of charge. Scheduled to run from 13h00 until 17h00, it is followed by the keynote address in the main auditorium at 18h00, and then the official opening of SA Heart Congress in the exhibition hall at 19h00.

Topics include:

    • Chest pain syndromes – when it is angina pectoris
    • Pharmacological treatment of heart failure with reduced EF
    • CAD in a patient with diabetes
    • Management of lipid disorders
    • Ethics: How to avoid litigation
    • Atrial fibrillation and stroke
    • An interactive ECG session

“As in the past, non-cardiologists will benefit by getting the most up-to-date information from leading experts regarding current drug use and practices in cardiology,” says HeFFSA vice-president, Dr Martin Mpe.  “The workshop will be interactive, and with a large percentage of patients unfortunately suffering from cardiovascular and hypertension related problems, the content will be of considerable benefit to their practices.”

To view the programme for SA Heart Congress, and to register for the pre-congress Cardio Update Workshop for non-cardiologists, visit www.saheart.org/congress2014. For queries, contact Europa Organisation Africa on (011) 325 0020, or email mandy@eoafrica.co.za.

Dedicated programme for paediatric cardiologists at SA Heart Congress 2014

Posted on Wednesday, 30 July 2014 14:01

There will be a pre-congress workshop on Peri-operative and Peri-interventional Transoesophageal Echocardiograhy (TOE) on Thursday, October 16th from 12h00 – 17h00. This will cover basic views, evaluation of congenital heart disease and ASD closures, as well as evaluation of the mitral valve. The AGM for the Paediatric Cardiac Society of South Africa (PCSSA) will be held immediately after the workshop from 17h00 – 18h00.

The 2014 SA Heart Congress has a dedicated and comprehensive programme for paediatric cardiologists that will be taking place daily at the International Conference Centre in Durban from Friday, October 17th through to Sunday, October 19th.

There will be a pre-congress workshop on Peri-operative and Peri-interventional Transoesophageal  Echocardiograhy (TOE) on Thursday, October 16th from 12h00 – 17h00. This will cover basic views, evaluation of congenital heart disease and ASD closures, as well as evaluation of the mitral valve. The AGM for the Paediatric Cardiac Society of South Africa (PCSSA) will be held immediately after the workshop from 17h00 – 18h00. 

Key topics designated for the paediatric cardiology track on Friday, October 17th include:
• Providing a service with limited resources (Dr Krishna Kumar, India)
• The status quo of paediatric cardiac services in South Africa (Dr Liesl Zühlke); and
• Making difficult decisions with limited resources.

Paediatric cardiologists will join the general plenary sessions on Friday afternoon for the session on valvular/structural heart disease.

On Saturday, October 18th, various aspects of congenital heart disease will be discussed in the morning by speakers who include Drs Krishna Kumar and Tim Jones (UK).  The afternoon session will focus on single ventricle physiology and will cover the evaluation and monitoring of patients over their lifetime, surgical techniques, and the anaesthetising and imaging of Fontan patients for non-cardiac procedures.

The morning of Sunday, October 19th has been dedicated to an interactive session covering some of the more challenging percutaneous interventions in congenital heart disease. This workshop will include:
• Percutaneous closure of peri-membranous VSDs
• Ballooning and stenting of branch pulmonary arteries
• Percutaneous closure of PDAs safely in infants below five kg; and
• PDA stenting.

For full programme details, and to register for SA Heart Congress and the pre-congress workshops, visit www.saheart.org/congress2014.  For queries, contact Europa Organisation Africa on (011) 325 0020, or email info@eoa.co.za

SA Heart congress 2014 allied

Posted on Thursday, 24 July 2014 14:09

Two pre-congress workshops of interest to allied professionals will be held on Thursday, 16th October. This will be followed by dedicated tracks for allied professionals on other congress days.

The 2014 SA Heart Congress includes an intensive and comprehensive programme for allied professionals. 

Two pre-congress workshops of interest to allied professionals will be held on Thursday, 16th October. This will be followed by dedicated tracks for allied professionals running from 13h30 – 17h00 on both Friday 17th and Saturday 18th October.

Allied professionals will also have the opportunity of attending the general plenary sessions being held at the congress on Friday, Saturday and Sunday mornings.  

On Thursday 16th October a joint pre-congress workshop on State of the Art Imaging will be conducted by members of both the prestigious Mayo Clinic and SA Heart. An alternative workshop on Peri-operative and Peri-interventional Transoesophageal Echocardiograhy (TOE) will be held simultaneously. 

Key topics covered in the track designated specifically for allied professionals on Friday, October 17th include the following:

• ECG interpretation in STEMI and NSTEMI
• AMI experience in thrombolysis and PPCI in both public and private settings
• Non-atherosclerotic causes of AMI
• The current role of GPllbllla
• Syntax score
• An update on the STEMI Early Reperfusion Project

The following topics will be addressed in the allied professionals’ track on Saturday 18th October:

• Challenges facing emergency medical services
• The presentation, discussion and review of three case studies
• Arrhythmias and pacing in an AMI setting
• The role of thrombectomy and PPCI
• Bleeding complications following AMI
• How IVUS/FFR/OCT can improve patient outcomes

SA Heart Congress is being held this year at the International Convention Centre in Durban. For full programme details, and to register for SA Heart Congress and the two pre-congress workshops, visit www.saheart.org/congress2014. For queries, contact Europa Organisation Africa on (011) 325 0020, or email info@eoa.co.za

SA Heart congress 2014

Posted on Friday, 18 July 2014 14:12

The 15th Annual SA Heart Congress will focus on bridging the divide between best practice and the challenges faced in implementing these ideals. To be held at the International Convention Centre in Durban, from 16 – 19 October, 2014, the congress will be hosting leading international faculty as well as local experts, and for the first time a dedicated team from the European Society of Cardiology (ESC). The ESC faculty will share some of the key clinical issues (hot topics) and late-breaking clinical trials from their recent 2014 congress.

Novel approaches in cardiovascular research

Although cardiovascular disease has always been at the forefront of research and development, course director, Dr Sajidah Khan, comments that innovation in the pharmacology domain has plateaued over the past decade. The opening plenary session will focus on novel approaches in CVD research, linking molecular science to clinical cardiology.

A new look at the basics and fundamentals

Not forgetting the basics, Dr Khan says that “Confusion has arisen in the ranks regarding basic entities such as what constitutes high blood pressure and what the therapeutic targets should be for treating high lipid levels”. The differing viewpoints will be discussed during one of the plenary sessions.

In addition, she points out that “Although cardiology is now very high tech on the one hand, on the other hand there is also a divergence of opinion with regard to fundamentals, such as what constitutes optimal nutrition for good cardiovascular health” – another congress topic. She hopes to generate healthy debate on the issue. The topical subject of nutriceuticals – and whether they have a role to play in cardiac health – is also earmarked for discussion. 

Current technology
To bring delegates up to speed with current technology, international faculty will present on the latest innovations in bio-absorbable scaffolding and renal denervation, as well as aspects of pacing and electrophysiology.

Heart transplants

The current status quo with regard to heart transplantation in South Africa, in both the public and private health sectors, should also generate much discussion.

Pre-congress workshops

In addition to the mainstream programme, pre-congress workshops on Thursday, October 16th, include the annual Cardiology Update for non-cardiologists; a Joint Mayo Clinic / SA Heart State of the Art Imaging Workshop; and a Peri-operative and Peri-interventional Transoesophageal Echocardiography (TOE) workshop by paediatric cardiologists.

Parallel sessions for Special Interest Groups and allied professionals

Parallel sessions of particular interest to special interest groups and allied professionals will focus on the areas of paediatric cardiology, cardiac arrhythmia, heart failure, cardiac imaging, cardiovascular research and cardiothoracic surgery.

A larger audience in 2014

The 2014 SA Heart Congress hopes to address a larger audience this year, with cardiac anaesthetists participating in a novel session titled “Let the team meet”.

“Medical professionals with a special interest in cardiovascular disease cannot afford to miss this congress,” Dr Khan concludes. “The faculty line-up is outstanding and they have condensed the most up-to-date information into just 3,5 days.  An added bonus is that Durban is one of the few cities in the world where you get a major urban metropolis located within a sub-tropical resort!”

For more information on the 2014 SA Heart Congress, visit  www.saheart.org/congresss2014, or contact Europa Organisation Africa on (011) 325 0020, or email: mandy@eoafrica.co.za

Thrombosis management

Posted on Wednesday, 18 June 2014 14:15

Bridging the divide at the 2014 Annual SA Heart Congress

Barcelona 13-14 June 2014
Feedback from Dr Tony Dalby


Attachments:

Thrombosis_2014_(2).pdf 443.1K 16 Apr 15 14:15

Cardiology at the limits

Posted on Tuesday, 6 May 2014 14:19

Dr Dalby attended the Cardiology, Nephrology and Diabetes at the Limits meeting in London and reports back:

 

Notes from the Front
“At the Limits”
London, 24 – 27 April 2014

An “At the Limits” meeting in Cardiology, Diabetes and Nephrology was held at the Royal College of Physicians in London this year.  All 15 previous meetings had been held in Cape Town.  The meeting was organised by Prof Lionel Opie and Prof Derek Yellon assisted by Prof John Cunningham, Prof Peter Libby, Prof Marc Pfeffer and Prof Brian Rayner   The meeting was held under the auspices of the Hatter Institute of University College London and the University of Cape Town.  Participating organisations were the the British Cardiovascular Society, the South African Heart Association, The Renal Association, the National Institute for Health Research and the Brigham and Womens’ Hospital.  The meeting was endorsed and supported by The Lancet. Sponsorship was provided by Novo Nordisk, AstraZeneca, Bristol-Myers Squibb, Pfizer, Amgen, Servier, Boehringer-Ingelheim, Bayer HealthCare, Daiichi-Sankyo, The Coca-Cola Company, MSD and Roche.  The meeting received Continuing Medical Education accreditation from the European Board for Accreditation in Cardiology (EBAC).

As has been the case at every previous meeting, an exceptionally high academic standard was maintained by all the presenters throughout the 4 days.  Lively audience participation after each presentation enhanced the learning experience.

Thursday

Prof M Pfeffer: Surprising findings from clinical trials

Prof Pfeffer reviewed a outcomes of trials in hypertension, dyslipidaemia (LDLc and HDLc), arrhythmias (CAST), LV dysfunction (with flosequinan and other positive inotropes) and HRT that have altered therapy.  These changes occurred because the clinical outcomes were made clear.  Unwarranted dependence on surrogate endpoints has misled treatment in the past.  Randomised controlled trials are needed to be able reach reasonable conclusions.  He remarked on the responsibility of the DSMB to be aware of the specific therapy being given to each group and not being blinded to the treatment allocation.  Treatment is adversely affected at times by direct to consumer advertising and clinical bias. As an example, the refusal of regulators and investigators to accept placebo control in TREAT (darbopoeitin alpha) was based on the premise that raising hemoglobin had to be beneficial.  Biomarkers and surrogate endpoints are aids to research but do not conclusively indicate the need to treat. Although certain treatments do not require randomised trials to prove their worth, in 1981 Braunwald wrote about not letting the genie out of the bottle (releasing new therapies for patient use) before outcomes research has been completed. 

Prof E Braunwald: Heart failure at the limits (The Lancet Lecture). 

Prof Braunwald spoke about the “war on heart failure.”  Although survival and quality of life have improved in chronic heart failure, heart failure with preserved ejection fraction (HeFPEF) and acute heart failure (AHF) remain a problem.  AHF has an 11% 30 day mortality.  Overall heart failure (HF) results in 1 million hospitalisation / year in the USA.

He discussed 5 novel promising treatment modalities in heart failure treatment:

1. MicroRNA binds to RNA and can suppress protein production.  MicroRNA’s may be useful biomarkers of heart failure and possible targets for treatment.  Inhibition of miR-25 (which is up-regulated in HF) improves cardiac contractility in the failing heart (Wahlquist, Nature, 2014).

2. Calcium cycling is involved in excitation-contraction coupling. The ryanodine receptor facilitates Ca entry into the sarcoplasm whereas the SERCA pump facilitates entry into sarcoplasmic reticulum. Phospholamban also important.  Calmodulin kinase II inhibition can reduce the increase in heart weight.

3. Gene therapy to incorporate DNA.  Adeno-associated viruses are of most interest.  It has been shown that calcium can be up-regulated in severe heart failure via SERCA with gene therapy. Persistent gene expression was noted up to 31 months after treatment.

4. Cell therapy using stem cells or progenitor cells.  REPAIR AMI showed improved LVEF and wall thickening at 2 years. In this research there is a lack of evidence of long term clinical benefit.  The BAMI trial is looking at post-reperfusion administration in patients with a left ventricular ejection fraction (LVEF) <45%, assessing survival at 2 years.

5. Left ventricular assist devices (LVAD): In the USA more than 75% of devices are used now as destination therapy and no longer as a bridge to transplant.  Research is proceeding on the HeartWare intrapericardial device that pumps 10 L/min.  Reverse remodeling has been documented over time with LVAD: some of the beneficial changes involve neurohormones, hypertrophy and calcium cycling.  Survival after explantation of LVAD may be excellent in many cases. Braunwald suggested intervention with an LVAD might be beneficial at an earlier stage in the development of heart failure. It will be necessary to explore how to eliminate transcutaneous leads to make the devices safer.

Finally he also noted the announcement of a trial involving an ARB (valsartan) and neprolysin that improved outcomes in chronic HF.  Neprolysin (LCZ696) inhibits BNP.

Friday

Prof Matthias Frick: Anti-platelet therapy

The focus of his talk was on acute coronary syndrome (ACS). Clopidogrel’s disadvantages include variability in response, delayed onset of action, polymorphisms and delayed offset of action.  Newer P2Y12 inhibitors have a more homogenous response. In PLATO ticagrelor was effective but also associated with an increase in bleeding. In STEMI with the new agents, results with the newer agents have been better than with clopidogrel and without increased bleeding. His concerns with the TRILOGY trial which compared prasugrel to clopidogrel in ACS patients not undergoing revascularisation included the high percentage of hypertensives and smokers and the low incidence of angiography. The ongoing ISAR REACT trial is studying ticagrelor vs. prasugrel. He proposed risk stratifying NSTEMI patients to choose the best P2Y12 for them according to their assessed bleeding risk.

Prof Vincente Torres: Aquaretics

Torres drew parallels between the humoral and intracellular responses in polycystic renal disease (vasopressin) and heart failure (catecholamines). The neurohypophysis receives preprovasopressin which is broken into a number of active substances. Vasopressin is secreted in low concentration to which CD Principal Cells are highly sensitive. With low BP a high concentration of vasopressin is secreted to which the receptors have a low sensitivity. Vaptans reduce water and salt retention, reduce cardiomyocyte senescence, reduce diuretic requirements, reduce natriuretic peptides and may be renal protective. Vaptans may not produce the neurohormonal response seen with furosemide. Vaptans may reduce myocardial fibrosis. However to date the clinical trials have been discouraging.  Mortality and HF hospitalisation were not improved. Post-marketing survey of tolvaptan in Japan has shown reduction in oedema, dyspnoea with sustained weight reduction and a stable serum sodium and creatinine. Thirst may be a limiting factor when using this treatment.

In polycystic kidney disease (PCKD), inhibition of vasopressin by tolvaptan has reduced the development of PCKD. It reduced the rate of decline in kidney function and reduced kidney pain. The effect size was bigger in those with worse kidney function at randomization.  The problem was the higher incidence of adverse events, including liver dysfunction which appeared to be restricted to the first 15 months of treatment.


Prof Lionel Opie: Are there cardiac benefits to red wine?

Modest alcohol is beneficial but the quantity required to achieve the effect is not definitely determined. Women are more susceptible to adverse effects of alcohol than men. The sex difference may relate to females’ HDLc level. A Danish study indicated that the alcohol benefit was confined to wine, not beer or spirits. Red wine intake inhibited tissue factor in pigs. Phasic thrombosis in dogs is inhibited by red wine (Circulation 2006). De-alcoholised red wine decreased ssystolic blood pressure (sBP) and diastolic blood pressure (dBP) through a nitric oxide (NO) mediated mechanism (Circ Res 2012). Resveratrol and melatonin in similar concentrations to those found in red wine protect against myocardial infarction (MI) and ischaemic reperfusion injury. He postulates that SAFE pathway is activated.  Melatonin is active in very small concentrations.  In an experimental situation melatonin protected against ischaemia. It is possible to block the effect of melatonin with luzindole (receptors 1 and 2). Both resveratrol and melatonin act through STAT-3 phosphorylation. 

Prof del Prato: The link between diabetes and cancer

There is plausible evidence to support a higher incidence of cancer in diabetes, especially liver cancer and T cell lymphoma (HR about 2.5X).  It should be regarded as a long term complication of diabetes. There is a link between fasting blood glucose and cancer (as with vascular deaths) (Emerging Risk Factors Collaboration. N Engl J Med, 2011, 364). Hyperglycaemia affects a number of pathways promoting cell proliferation and survival and activate pro-inflammatory pathways.  Hyperglycaemic memory facilitates breast cancer growth. Hyperglycaemia can induce resistance to chemotherapy in prostate cancer cells.  Insulin aggravates the tendency; there are suggestions that longer acting insulins may be worse.  Subjects in the ORIGIN trial did not show an increased cancer risk.  Gerstein commented that the absolute risk of cancer in ORIGIN was higher than the risk of CVD.

Prof Sir Rory Collins: LDL cholesterol – how low can we go? (The South African Heart Association and British Cardiovascular Society Lecture)

The importance of cholesterol was initially underestimated due to lack of a global perspective on population lipid levels. Statin treatment vs. control yields approximately 20% reduction in CV events.  There is a lag phase after starting treatment (50% of total effect) with incremental improvement year-on-year (about ¼).  There is a potential for greater benefit with early intervention. The allegations of unacceptable % of side-effects from statins is a misrepresentation. Statin side effects were reviwed by Kashoni (Circulation, 2006).  There has been no emergence of cancer over longer term observation. New onset diabetes is increased (HR 1.09).  There is no evidence of memory loss nor evidence for cataract development (HR 1.01)  in the Health Protection Study. Trials of more vs. less potent statin therapy showed a greater benefit for the more potent treatment arm.  The IMPROVE IT trial result comparing simvastatin + ezetimibe to simvastatin in patients after ACS awaited. Trials with cholesterol ester transfer protein (CETP) inhibitors that raise HDL are in progress as are outcome trials of PCSK9 inhibitors.

Prof Hertzel Gerstein:   Vasculopaenia in diabetes

Diabetes mellitus (DM) is a disease of accelerated aging; there are legion complications of diabetes.  The risk of complications increases below the glucose threshold at which diabetes is diagnosed.  Tighter control of glucose reduces eye disease, albuminuria, MI (but no overall effect on major cardiovascular events). In T2DM the presence of retinopathy increases the risk of death 2.4X.  In ACCORD progressive retinopathy predicted higher mortality. Diabetes rarifies the vasa vasorum.  Albuminuria may not be specific to DM.  Yaqoob noted that while the blood glucose is persistently elevated  in glucose 6 phosphate deficiency, it does not result in vascular complications.

Prof N Morrell:  Pulmonary hypertension

PHT may be due to “idiopathic” PAH or may accompany left heart disease, lung disease, PTED or rarer causes such as sarcoidosis or histiocytosis. IPAH may be truly idiopathic, familial, drug-induced, related to HIV or autoimmune disorder. Endothelin (ET) antagonists, NO pathway activation (by PDE5 inhibition) and prostacyclin derivatives have been used in treating the condition.  These agents have provided symptomatic relief and possibly improve survival but mortality remains high.

The familial condition is an autosomal dominant with poor penetrance (about 20%). A  bone morphogenic protein BMPR2 encodes a tissue growth factor- beta (TGF-beta) receptor. Numerous forms of mutation leading to loss of function.  15-26% of cases are sporadic mutations.  Mutations have been found in 19% of idiopathic PAH and 77% in the familial group.  BMPR2 has been shown to be reduced in lung tissue in familial and idiopathic PHT.Inflammation in BMPR2 deficient individuals leads to breakdown of endothelium and smooth muscle cell proliferation.  BMP9 reverses pulmonary hypertension in experimental mice.  Chloroquine inhibits the lysosomal degradation of BMPR2.  

Patients who have heart or lung disease with disproportionate PHT may have an underlying genetic predisposition.

Prof D Raal:  The future beyond statins: novel lipid-lowering drugs (The Hatter Award Lecture)

There is an unmet need in the treatment of familial hypercholesterolaemic (FH) patients because maximised statin therapy fails to lower LDL cholesterol sufficiently.  Although the mortality of FH patients has improved since the introduction of statins, FH patients still suffer cardiovascular events and die prematurely.  Prof Raal explored the alternatives to statin therapy which might overcome this problem.  
1. Mipomersin is an antisense which blocks ApoB production inhibits VLDL and thus LDL production. In a trial mipomersin reduced LDL by 25%. However there were problems with injection site reactions and ‘flu-like symptoms. 
2. Microsomal triglyceride transfer protein (MTP) inhibition with lopitamide also inhibits VLDL production.  LDL was reduced up to 50% but liver enzymes were increased.
3. PCSK9 regulates cellular LDL uptake. Currently all the front runners in this area are injectable monoclonal antibodies.  These agents produce a significant sustained reduction in LDLc and Lp(a) in heterozygous FH. His patients with homozygous FH showed a variable but significant response in LDLc.  Theoretically, the side effects of PCSK9 inhibition might include hepatic, pancreatic, neurocognitive and glycaemic problems. 
4. Raal was not optimistic about the prospects for CETP inhibitors.

Saturday:

Prof G Mancia: Micro- and macrovascular events in diabetes and hypertension

BP control in DM (BMJ 1998; 317, 703) reduces cardiovascular events.  The variety of drugs were used in the various trials in hypertensive diabetics all achieved the same result.  There were no significant differences in outcome between various agents used to control BP.  There is a linear relationship between magnitude of BP reduction and reduction in cardiovascular (CV) events. A beneficial effect has been noted in only one trial in DM that reduced BP below 130 mm Hg. In a post-hoc analysis of  VALUE, reducing BP <130 mm Hg showed no benefit.  Benefit has been demonstrated only in the range <140 mm Hg >130 mm Hg.  Mancia recommends using 140/85 as a target in diabetics.  In ACCORD serious adverse events were 3X higher with aggressive BP reduction (<120 mm Hg).  Adherence to prescription was associated with reduction in both coronary and cerebrovascular events (Lombardy study). It is difficult to get sBP controlled in DM. The totality of evidence supporting reduction in the frequency of MI with antihypertensive treatment is not convincing. Angiotensin receptor blockers (ARBs) provide better protection against progression of nephropathy.  In ADVANCE there was no effect in DM on deterioration in vision, neuropathy, dementia and cognitive decline.  The optimal BP target may vary between and within patients.  The coronary perfusion in patients with LVH may be more sensitive to reduction in BP than patients without LVH. It was proposed that borderline BP elevations be treated only if significant global risk is present. Even sub-optimal BP control provides substantial CV protection.  A wide pulse pressure is a marker of risk, but there is no convincing evidence to support specific management.

Prof M Yaqoob: Uraemic LVH    

Myocardial disease is the major cause of death in uraemia, accounting for around a third of the mortality.  When presenting for dialysis only 10% of patients have a normal echocardiogram.  90% have HT when starting dialysis and most have poor BP control.  However the histology of uraemic left ventricular hypertrophy (LVH) is different to that encountered  in HT.  Histology reveals more fibrosis and more capillary drop-out.  These changes are akin to the senescent heart or the findings in progeria.  The CV mortality of young patients on haemodialysis is equivalent to that of octogenarians.   Yaqoob considers the process to be that of premature aging.  Progerin (prelamin A) is implicated. Autophagy allows for recycling of damaged cells and its inhibition leads to premature aging.  In normotensive uraemia there is downreglation of genes promoting autophagy.  The arterial stiffness present in normotensive uraemic patients is reversed by angiotensin converting enzyme inhibition (ACEI) but unresponsive to NO.  Uraemia per se (without HT or anaemia) results in LVH. Calpain which hydrolyses the cell skeleton is increased in uraemia.  It may be the cause of low grade myonecrosis and the reason for the elevation of troponin seen in kidney failure.  Uraemic patients sustain larger MI’s and higher mortality.  Ouabain is elevated in uraemia and promotes calpain activity. FGF23 is phosphaturic and is secreted even in earlier stages of kidney injury and promotes LVH.

Prof C Granger: Atrial fibrillation

Only 50-60% of patients with AF are anti-coagulated. 

The LA appendage occluder may offer an alternative to anticoagulation in patients unable to or unwilling to take an anticoagulant.  However, less than 40 strokes were observed in the Watchman trials and though there were fewer strokes with than without the device the numbers are too few to draw firm conclusions about its effectiveness. 

The meta-analysis by Ruff (Lancet 2013) of the results with NOAC’s showed a 50% reduction in haemorrhagic stroke and 10% reduction in  mortality.  Treatment effects across the age range were consistent.  NOAC’s are better tolerated than aspirin and cause less intracranial haemorrhage than aspirin (AVERROES). 

Prof V Fuster:  Imaging and screening of sub-clinical diseases: is multimodality exceeding the limits? (The NIHR-UCLH Biomedical Research Centre Lecture)

Fuster spoke of the need for the profession to transition from the treatment of disease to the maintenance of health.  His group has used carotid 3D ultrasound and coronary calcium to study 6 000 healthy middle-aged patients.   These studies demonstrated a close interaction between carotid and coronary disease.  Carotid IMT was not highly as predictive.  They found that a significant number with a low Framingham risk score had established disease.  Multimodal imaging identified patients at a higher short term risk than their Framingham score indicated although their longer term risk may be equivalent to their risk calculted with Framingham.  Fuster holds that the concept of “vulnerable plaque” is not valid. In his study, patients knowing their findings did not improve their treatment adherence.  In the Spanish study of a younger group of patients,  ilio-femoral changes were more sensitive than carotid changes in detecting disease.  Over time rapid progression of disease from single to multiple sites was documented.  Once again, in this younger group of patients, disease was found in around 40% of subjects who had a low Framingham risk score. MRI scans identified lacunar infarcts  due to small vessel occlusion in patients with identifiable disease.  The CARDIA study showed that eventual cognitive dysfunction relates to risk factors that are present in young middle age. Telomere function affects the aging process.  As the telomere shortens cell renewal decreases.  Senescence associated factors promote many of the features associated with advanced age.

Sunday

Prof P McCullough: Pathogenesis of acute cardiorenal syndrome

There are 5 subdivisions of the cardiorenal syndrome (CRS). 1. Acute cardiac failure, 2. Chronic heart failure determining progressive kidney injury, 3. Acute kidney dysfunction, 4. Chronic kidney injury, 5. Combination disorders.  50-78% of acute kidney injury (AKI) is community acquired.  The calcium disorder in AKI also leads to calcium deposition in the myocardium. Albuminuria is pathogenic in AKI; urinary protein impairs repair of the glomerular injury. Also renal venous congestion plays an important role in the deterioration of kidney function. 30% of AKI results in permanent dysfunction. TIMP-2 and IGFBP7 are cell cycle arrest markers that appear in the urine with early kidney injury. Renal resistance to diuretics is occurring at multiple levels in the kidney.  None of the clinical trials have demonstrated an effective general strategy to manage CRS Type 1.  McCullough recommends identifying the patient phenotype according to the wet-dry and warm-cold 2X2 division previously proposed by Warner Stevenson.

Prof. L Warner Stevenson: Therapy of acute CRS

Patients are living longer with HF today. Consequently there has been a concomitant increase in kidney failure.  Over time the diuretic doses used in HF have increased also.  Most HF symptoms are improved when the LVEDP <25 mm Hg.  Aggravated kidney dysfunction is almost never associated with a fall in cardiac output.  CRS is equally common in HeFPEF and heart failure with reduced ejection fraction (HeFREF).  Diuretics decrease the incidence of HF in HT.  Neither dopamine or neseritide improved diuresis.  Ultrafiltration in UNLOAD reduced 90 day hospitalisation (Constanzo, JACC, 2009). However in CARESS (Bart, NEJM, 2012) there was no difference in 60 day mortality with more adverse effects.  Acute worsening of kidney function is probably a reflection of underlying chronic kidney injury.  Haemoconcentration worsened kidney function but had better outcomes.  In-hospital decongestion results in only 33% staying decongested at 30 days.  The outcome of left venricular assist device (LVAD) implantation is influenced by baseline kidney function.  The CHAMPION trial showed reduced hospitalisation by adjusting diuretic therapy according to haemodynamic monitoring (Ritzema, Circulation, 2010) – 2/3 of adjustments were to reduce diuretic dose and was accompanied by increase in neurohormonal therapy.  She advised against trying to shorten the length of stay by using ultrafiltration.


Attachments:

at_the_limits_logo__580_190_80_s.jpg 17.4K 16 Apr 15 14:19

Feedback on ACC 2014

Posted on Sunday, 20 April 2014 14:23

Dr Dalby reports

Dr Dalby reports from his recent trip to the ACC 2014 conference


Attachments:

ACC_14_REPORT_SA_Heart.pdf 257.6K 16 Apr 15 14:23

SA Heart on Wouter Basson

Posted on Monday, 24 February 2014 14:26

SA Heart does not condone unethical behavior of any kind.

The South African Heart Association (SA Heart) is a body aiming to promote the science, education, professional interest and fellowship of health care workers in the sphere of cardiovascular health in South Africa.  This includes support for and maintenance of standards for quality health care.

The Health Professional Council of SA is the body tasked with the maintenance of health care standards and protection of the public in matters of health care in South Africa.  

After following due process, the HSPCA found Dr Wouter Basson guilty of unethical behavior. SA Heart upholds the finding of the Health Professional council of SA on Dr Wouter Basson.

SA Heart does not condone unethical behavior of any kind.

Dr Wouter Basson is not a member or the SA Heart Association, and his unethical conduct occurred prior to his qualification as a cardiologist and his involvement with cardiovascular care.


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