Philip Herbst
Stellenbosch University
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Featured researches published by Philip Herbst.
Circulation | 2011
Hellmuth Weich; J.T. Janson; Jacques van Wyk; Philip Herbst; Pieter le Roux; Anton Doubell
The patient is a 38-year-old woman with rheumatic heart disease requiring surgery 21 years ago. She received a St. Jude mechanical prosthesis in the mitral position and a Carpentier-Edwards Perimount bioprosthesis (size 31) in the tricuspid position. Over the past 2 years, she has become progressively more short of breath with regular admissions for congestive heart failure despite medical treatment. Transthoracic echocardiography showed a severely dilated right atrium and a calcified tricuspid prosthesis with a mean gradient across the valve varying between 9 and 12 mm Hg (Figures 1 and 2). The mitral valve prosthesis functioned well. Figure 1. The continuous wave spectral Doppler of the degenerate tricuspid prosthesis before the procedure showing a profile of severe tricuspid stenosis with averaged (because of atrial fibrillation) peak and mean gradients of 12 and 9, respectively. Vmax indicates maximum flow velocity; Vmean, mean flow velocity; Pmax, maximal pressure gradient: Pmean, mean pressure gradient; Env Ti, duration of measured envelope; VTI, velocity time integral; HR, heart rate. Figure 2. Pressure half-time (PHT) measured over the tricuspid valve confirms severe tricuspid stenosis with a value of 461 ms. A decision was made to replace the tricuspid valve, but in consultation with the heart team, it was agreed that, given that the mitral valve prosthesis was functioning well, the risk of a second sternotomy to replace only the tricuspid valve was difficult to justify if an alternative option was available. Given the limited lifespan of a bioprosthesis in a young person, she would then require her third (and likely final) sternotomy at a young age. A joint decision was therefore made to offer the patient a minimally invasive tricuspid valve replacement by a transcatheter procedure. The risks of a transcatheter procedure were discussed with her, and she provided written informed consent. The option of a …
Annals of Pediatric Cardiology | 2017
Scott Dougherty; Maziar Khorsandi; Philip Herbst
Rheumatic heart disease (RHD) is a disease of poverty, is almost entirely preventable, and is the most common cardiovascular disease worldwide in those under 25 years. RHD is caused by acute rheumatic fever (ARF) which typically results in cumulative valvular lesions that may present clinically after a number of years of subclinical disease. Therapeutic interventions, therefore, typically focus on preventing subsequent ARF episodes (with penicillin prophylaxis). However, not all patients with ARF develop symptoms and not all symptomatic cases present to a physician or are correctly diagnosed. Therefore, if we hope to control ARF and RHD at the population level, we need a more reliable discriminator of subclinical disease. Recent studies have examined the utility of echocardiographic screening, which is far superior to auscultation at detecting RHD. However, there are many concerns surrounding this approach. Despite the introduction of the World Heart Federation diagnostic criteria in 2012, we still do not really know what constitutes the most subtle changes of RHD by echocardiography. This poses serious problems regarding whom to treat and what to do with the rest, both important decisions with widespread implications for already stretched health-care systems. In addition, issues ranging from improving the uptake of penicillin prophylaxis in ARF/RHD-positive patients, improving portable echocardiographic equipment, understanding the natural history of subclinical RHD and how it might respond to penicillin, and developing simplified diagnostic criteria that can be applied by nonexperts, all need to be effectively tackled before routine widespread screening for RHD can be endorsed.
Cardiovascular Journal of Africa | 2015
Jomien Mouton; Adriano S Pellizzon; Althea Goosen; Craig J. Kinnear; Philip Herbst; Paul A. Brink; Johanna C. Moolman-Smook
Summary Introduction The minimum criterion for the diagnosis of hypertrophic cardiomyopathy (HCM) is thickening of the left ventricular wall, typically in an asymmetrical or focal fashion, and it requires no functional deficit. Using this criterion, we identified a family with four affected individuals and a single unrelated individual essentially with restrictive cardiomyopathy (RCM). Mutations in genes coding for the thin filaments of cardiac muscle have been described in RCM and HCM with ‘restrictive features’. One such gene encodes for cardiac troponin I (TNNI3), a sub-unit of the troponin complex involved in the regulation of striated muscle contraction. We hypothesised that mutations in TNNI3 could underlie this particular phenotype, and we therefore screened TNNI3 for mutations in 115 HCM probands. Methods Clinical investigation involved examination, echocardiography, chest X-ray and an electrocardiogram of both the index cases and close relatives. The study cohort consisted of 113 South African HCM probands, with and without known founder HCM mutations, and 100 ethnically matched control individuals. Mutation screening of TNNI3 for disease-causing mutations were performed using high-resolution melt (HRM) analysis. Results HRM analyses identified three previously described HCM-causing mutations (p.Pro82Ser, p.Arg162Gln, p.Arg170Gln) and a novel exonic variant (p.Leu144His). A previous study involving the same amino acid identified a p.Leu144Gln mutation in a patient presenting with RCM, with clinical features of HCM. We observed the novel p.Leu144His mutation in three siblings with clinical RCM and varying degrees of ventricular hypertrophy. The isolated index case with the de novo p.Arg170Gln mutation presented with a similar phenotype. Both mutations were absent in a healthy control group. Conclusion We have identified a novel disease-causing p.Leu144His mutation and a de novo p.Arg170Gln mutation associated with RCM and focal ventricular hypertrophy, often below the typical diagnostic threshold for HCM. Our study provides information regarding TNNI3 mutations underlying RCM in contrast to other causes of a similar presentation, such as constrictive pericarditis or infiltration of cardiac muscle, all with marked right-sided cardiac manifestations. This study therefore highlights the need for extensive mutation screening of genes encoding for sarcomeric proteins, such as TNNI3 to identify the underlying cause of this particular phenotype.
The Egyptian Heart Journal | 2017
Philip Herbst
This focussed review describes important problems experienced in the world of echocardiographic screening for asymptomatic rheumatic heart disease (RHD). It offers a critical appraisal of the screening criteria and their application and explores some of the fundamental principles underpinning the shortcomings of individual criteria. The author illustrates important mechanisms that underlie the morphological changes seen in RHD that must be accounted for if these criteria are to be rationalised and improved upon.
Echo research and practice | 2017
Annari van Rensburg; Philip Herbst; Anton Doubell
The therapeutic implications of bicuspid aortic valve associations have come under scrutiny in the transcatheter aortic valve implantation era. We evaluate the spectrum of mitral valve disease in patients with bicuspid aortic valves to determine the need for closer echocardiographic scrutiny/follow-up of the mitral valve. A retrospective analysis of echocardiograms done at a referral hospital over five years was conducted in patients with bicuspid aortic valves with special attention to congenital abnormalities of the mitral valve. One hundred and forty patients with a bicuspid aortic valve were included. A congenital mitral valve abnormality was present in eight (5.7%, P = 0.01) with a parachute mitral valve in four (2.8%), an accessory mitral valve leaflet in one (0.7%), mitral valve prolapse in one, a cleft in one and the novel finding of a trileaflet mitral valve in one. Minor abnormalities included an elongated anterior mitral valve leaflet (P < 0.001), the increased incidence of physiological mitral regurgitation (P < 0.001), abnormal papillary muscles (P = 0.002) and an additional chord or tendon in the left ventricle cavity (P = 0.007). Mitral valve abnormalities occur more commonly in patients with bicuspid aortic valves than matched healthy individuals. The study confirms that abnormalities in these patients extend beyond the aorta. These abnormalities did not have a significant functional effect.
Journal of Cardiovascular Ultrasound | 2016
Pieter van der Bijl; Philip Herbst; Anton Doubell
Background Effusive-constrictive pericarditis (ECP) is traditionally diagnosed by using the expensive and invasive technique of direct pressure measurements in the pericardial space and the right atrium. The aim of this study was to assess the diagnostic role of echocardiography in tuberculous ECP. Methods Intrapericardial and right atrial pressures were measured pre- and post-pericardiocentesis, and right ventricular and left ventricular pressures were measured post-pericardiocentesis in patients with tuberculous pericardial effusions. Echocardiography was performed post-pericardiocentesis. Traditional, pressure-based diagnostic criteria were compared with post-pericardiocentesis systolic discordance and echocardiographic evidence of constriction. Results Thirty-two patients with tuberculous pericardial disease were included. Sixteen had ventricular discordance (invasively measured), 16 had ECP as measured by intrapericardial and right atrial invasive pressure measurements and 17 had ECP determined echocardiographically. The sensitivity and specificity of pressure-guided measurements (compared with discordance) for the diagnosis of ECP were both 56%. The positive and negative predictive values were both 56%. The sensitivity of echocardiography (compared with discordance) for the diagnosis of ECP was 81% and the specificity 75%, while the positive and the negative predictive values were 76% and 80%, respectively. Conclusion Echocardiography shows a better diagnostic performance than invasive, pressure-based measurements for the diagnosis of ECP when both these techniques are compared with the gold standard of invasively measured systolic discordance.
The Egyptian Heart Journal | 2017
Annari van Rensburg; Charles Kyriakakis; Alfonso Pecoraro; Philip Herbst
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The Egyptian Heart Journal | 2017
Alfonso Pecoraro; Anton Doubell; Philip Herbst
An 83-year-old lady presented to our cardiac unit with presyncope and progressive dyspnoea.She had a regular bradycardia of 36 beats per minute with a slow-rising central pulse and normal jugular venous pressure without cannon A waves. Auscultation revealed a late-peaking, ejection systolic murmur (ESM) and soft second heart sound in keeping with severe aortic stenosis (AS). Interestingly, 2 added diastolic heart sounds were noted. A phonocardiogram with a simultaneous electrocardiogram (ECG) recording was undertaken using a mobile device. This revealed an early diastolic heart sound following a non-conducted P wave (S4x) in addition to a pre-systolic atrial heart sound (S4) and ESM (Panel A).
The Annals of Thoracic Surgery | 2017
Jacques T. Janson; André Coetzee; Gawie J. Rossouw; Izak Loftus; Adriaan Albertus Murray; Pieter Rossouw; Philip Herbst
BACKGROUND This study evaluated the use of an autologous vein graft, supported by expanded polytetrafluoroethylene (ePTFE) chordae tendineae, to replace an anterior mitral valve leaflet. METHODS A double-layered autologous jugular vein graft, supported by ePTFE chords, was used to create an anterior mitral valve leaflet in 21 sheep. Mitral valve function was monitored with echocardiography for up to 10 months. Surviving sheep were euthanized between 6 and 10 months later, and vein implants were examined histologically. RESULTS One sheep died intraoperatively. Fourteen sheep had trace to mild mitral regurgitation (MR), 5 had mild to moderate MR, and 1 had moderate to severe MR. Ten sheep died between 2 days and 6.2 months. Echocardiography at 6 months showed MR progression in 8 of 11 sheep. The vein leaflet developed intimal fibroplasia and fibrous proliferation in response to the increased stress on the tissue, but the vein remained flexible without shortening or contracture. The 6- to 10-month vein implants showed viability with intact endothelium, myofibroblasts, collagen, and elastin. A normal healing pattern was seen at the suture lines, and no calcification was observed in the vein leaflet apart from the ePTFE sutures. CONCLUSIONS Autologous vein has the potential to function as a mitral valve leaflet substitute because it adapted morphologically and remained viable in the intracardiac position. Technical refinement in creating and implanting the leaflet is needed to improve the progression of MR.
The Egyptian Heart Journal | 2014
Jane Moses; Charles Kyriakakis; Hellmuth Weich; Pieter Rossouw; Philip Herbst; Anton Doubell
A persistant left superior vena cava (PLSVC) draining to the coronary sinus (CS) is the most common venous anomaly of the thorax, affecting approximately 0.5% - 2% of the general population, and is present in up to 10% of patients with other congenital cardiac anomalies.(1) The embryological development of the thoracic venous system is complex and subject to significant variation. Usually, most of the left cardinal system involutes, leaving only the coronary sinus, which drains the cardiac veins, and the ligament of Marshall (a remnant of the left superior vena cava).(2) The presence of a PLSVC is usually an incidental finding at either echocardiography, cardiac catheterisation or device implantation.(1) The typical echocardiographic findings are that of a dilated CS, which can be appreciated on the parasternal long axis view, the parasternal short axis at mitral valve level, the apical 2 chamber view and a modified apical four chamber view scanning down to visualise the CS (Figure 1). A contrast study with agitated saline (“bubble study”) done via the left brachial vein will demonstrate the dilated CS draining into the right atrium (Figure 2).