rss

Recent eLetters

Displaying 1-10 letters out of 703 published

  1. Misinterpretation risks with a superficial reading of a meta-analysis. Reply to the letter by Nairooz et al.

    Nairooz and Naidu [1] claim that definitions of complete and non- complete MV-PCI in our meta-analysis[2] (multivessel percutaneous coronary intervention) might have been missed or misinterpreted in one included study. As a matter of fact, CvLPRIT trial randomized STEMI (ST-elevation myocardial infarction) patients to either complete revascularization (including all N-IRAs [non-infarct related artery]) or IRA-only treatment. Indeed, by study design, complete revascularization was recommended during index procedure, truly reflecting the inclusion criteria of our meta- analysis. Nairooz and Naidu are once more wrong when they argue that different time frames between index PCI and second procedure across the studies might have influenced the outcomes. While small number of studies conducted so far precludes detailed analyses, to assess the optimal timing of the second procedure, was not indeed the objective of the current meta- analysis. Nairooz and Naidu claim that staged PCI became anyhow bundled in the same group with IRA-only revascularization. These patients are similarly different to complete MV-PCI; indeed, the risk of MI in the IRA- only treated patients accrues over time; a difference in time in this group is pivotal also to demonstrate the impact of leaving a non culprit plaque untreated; the approach in our analysis therefore reflects the true clinical practice and indeed is based on coronary- and risk profile evaluation of the patients with non culprit plaques. An arbitrary,fixed time-frame second revascularisation for all patients with non culprit lesions is not only infeasible in clinical setting but ,indeed, dangerous treating in the same way patients with different coronary artery lesions; as a sensitivity analysis, a stratified meta-analysis by intervention in the control group was performed as well and results reported, showing consistency of results. Our study was not designed to compare same setting complete revascularization (CR) vs index hospitalization CR vs later date CR vs IRA only revascularization; neither was any study conducted to date. The criticism about methodology or clinical meaningfulness of a meta- analysis should be based upon specific clinical knowledge of the topic, and, above all, careful reading of the meta-analysis design.

    References:

    1. Nairooz R, Naidu SS. Complete revascularization in STEMI. Heart 2015 [Epub ahead of print] 2. Kowalewski M, Schulze V, Berti S, et al. Complete revascularisation in ST-elevation myocardial infarction and multivessel disease: meta-analysis of randomised controlled trials. Heart. 2015 Jun 2.

    Conflict of Interest:

    None declared

    Read all letters published for this article

    Submit response
  2. Re:Ischaemic conditioning: paving the pathway to clinical translation

    We thank Iliodromitis and colleagues for their interest in our review article1. Providing a comprehensive account of the extensive literature in this field has been a very challenging task. We are aware of their previous work2 3 on the feasibility of ischaemic postconditioning (IPost) in acute coronary syndrome. Of note, this was a small study of 37 patients and only included a total of 6 patients with non-ST elevation myocardial infarction (NSTEMI)2 3. To our knowledge no other study has since investigated the role of IPost in a larger cohort of NSTEMI. Therefore, IPost was not included under NSTEMI in Figure 2 of our review article1 as it has not been investigated in adequately powered studies for us to draw any meaningful conclusions. With regards to the second point raised, we acknowledge that the first study was by the authors' group4 investigating the role of remote ischaemic preconditioning (RIPC) in 40 patients, measuring serum cardiac enzymes as a marker for peri-procedural myocardial injury and they actually demonstrated RIPC-induced myocardial injury. As their study was probably underpowered, the findings should be interpreted with caution. In retrospect, we should have made this clearer in the table of "major" clinical studies in the review article1. The translation of ischaemic conditioning has been challenging and we entirely support the authors' view that all pieces of evidence in this field need to be taken into consideration and critically appraised in order to pave the transition of this intervention from bench to bedside in suitable clinical setting.

    1. Bulluck H, Hausenloy DJ. Ischaemic conditioning: are we there yet? Heart 2015;101(13):1067-77. 2. Iliodromitis EK, Paraskevaidis IA, Fountoulaki K, et al. Staccato reperfusion prevents reperfusion injury in patients undergoing coronary angioplasty: a 1-year follow-up pilot study. Atherosclerosis 2009;204(2):497-502. 3. Ikonomidis I, Iliodromitis EK, Tzortzis S, et al. Staccato reperfusion improves myocardial microcirculatory function and long-term left ventricular remodelling: a randomised contrast echocardiography study. Heart 2010;96(23):1898-903. 4. Iliodromitis EK, Kyrzopoulos S, Paraskevaidis IA, et al. Increased C reactive protein and cardiac enzyme levels after coronary stent implantation. Is there protection by remote ischaemic preconditioning? Heart 2006;92(12):1821-6.

    Conflict of Interest:

    None declared

    Read all letters published for this article

    Submit response
  3. Radiation exposure considerations relevant to using propofol for nurse-led sedation in cardiological practice

    The authors should be congratulated for providing timely guidance about the use of propofol for nurse-led sedation in modern cardiological practice.[1] The broad scope of the article surely prevented presentation of a comprehensive set of recommendations. However, a particularly important issue for the nursing staff who would be involved, which was not addressed in this article, deserves focused attention. A recent study reported that anaesthetists' radiation exposure is higher when sedation is used in comparison to general anaesthesia during cardiological procedures.[2] The reason radiation exposure was higher during sedation was the increased time spent in closer contact with the patient without additional shielding in circumstances where patients required manual ventilation or airway support.[2] Although radiation exposure was not specifically addressed in the previous reports of nurse-led propofol sedation for cardiological procedures that were cited by Furniss and Sneyd in their article1, nurses were required to support obstructed airways by applying jaw support and it was also reported that a small proportion of participants required manual ventilation in all of the studies. Therefore, there is the potential that nursing staff might be exposed to higher doses of radiation if nurse-led sedation with propofol is used during cardiological procedures in the place of general anaesthesia. For this reason, it would seem prudent to put systems in place to minimise radiation exposure as much as possible for nursing staff involved in nurse-led propofol sedation during cardiological procedures. It was recently reported that real-time radiation dosimeters reduced radiation exposure for anaesthetists during interventional radiology procedures.[3] Although further research would be required for confirmation, such technology may also be of use when propofol is used for nurse-led sedation in cardiological practice. 1. Furniss SS and Sneyd JR. Safe sedation in modern cardiological practice. Heart. 2015. doi:10.1136/heartjnl-2015-307656 2. Andreoli S, Moretti R, Lorini FL and Lagrotta M. RADIATION EXPOSURE OF AN ANAESTHESIOLOGIST IN CATHETERISATION AND ELECTROPHYSIOLOGICAL CARDIAC PROCEDURES. Radiation protection dosimetry. 2015. doi: 10.1093/rpd/ncv009 3. Baumann F, Katzen BT, Carelsen B, Diehm N, Benenati JF and Pe?a CS. The Effect of Realtime Monitoring on Dose Exposure to Staff Within an Interventional Radiology Setting. Cardiovascular and interventional radiology. 2015: 1-7. DOI: 10.1007/s00270-015-1075-6

    Conflict of Interest:

    None declared

    Read all letters published for this article

    Submit response
  4. Re: "There Truly is an Obesity Paradox"

    I appreciate Dr. Stovitz's interest in our editorial and on the topic of the "Obesity Paradox". As I stated in my book, The Obesity Paradox,1 a paradox can be defined "as a statement that is seemingly contradictory or opposed to common sense and yet is perhaps true". Based on this, Stovitz could have better titled his letter as "True, true, and is a true paradox." As we previously demonstrated,2-4 despite that obese with coronary heart disease (CHD) appeared to have a worse CHD risk profile, including more abnormal lipids , more adverse glucose and blood pressure values, and higher levels of inflammation, all of which suggest a worse prognosis, the prognosis of the overweight/ obese with CHD was "paradoxically" better. We believe that the fact that the obese were a few years younger than their leaner counterparts with CHD did not completely explain, or statistically explain, their better prognosis, which represents a true paradox. However, no pun intended, I believe that the rest of the letter by Dr. Stovitz is "true".

    As we stated in our editorial, "supporting the obesity paradox, however, does not mean that obesity is being promoted or that one is suggesting that obesity is a good thing." As we also stated, "quite possibly, many overweight and obese patients with CHD may not have developed CHD in the first place had obesity been prevented." On the other hand, although lean patients with CHD appear "healthier" than their overweight/obese counterparts with similar CHD, they have a worse prognosis, probably due to developing CHD from a different etiology, as Dr. Stovitz suggests, which I believe is due to genetic predisposition.

    Finally, as I started my editorial with the two CHD cases, one with BMI of 23 kg/m2 and the other with BMI 32 kg/m2, my points of the editorial remain true. Although many years ago I predicted that the thin patient with CHD would have a better prognosis, fifteen years later the data continues to show that overweight and obese (at least mildly obese) with CHD "paradoxically" have a better short- and medium-term prognosis.

    References: 1. Lavie CJ (with Loberg K). The Obesity Paradox - When Thinner Means Sicker and Heavier Means Healthier. New York, NY:Hudson Street Press;2014. 2. Lavie CJ, Milani RV, Artham SM, Patel DA, Ventura HO. The obesity paradox, weight loss, and coronary disease. Am J Med 2009;122:1106-1114. 3. Lavie CJ, De Schutter A, Patel D, Artham SM, Milani RV. Body composition and coronary heart disease mortality - an obesity or a lean paradox? Mayo Clin Proc 2011;86(9):857-864. 4. Lavie CJ, De Schutter A, Patel DA, Romero-Corral A, Artham SM, Milani RV. Body composition and survival in stable coronary heart disease. Impact of lean mass index and body fat in the "obesity paradox". J Am Coll Cardiol 2012;60(15):1374-80.

    Conflict of Interest:

    I am the author of the book "The Obesity Paradox" and I have served as a consultant and speaker for the Coca-Cola Company, but on fitness and not any of their products.

    Read all letters published for this article

    Submit response
  5. Ischaemic conditioning: paving the pathway to clinical translation

    The timely restoration of flow in the culprit coronary artery lesion remains the cornerstone of treatment in patients with evolving myocardial infarction but with the inevitable cost of reperfusion injury. Cardiac ischaemic conditioning (IC) is capable of reducing the extent of final infarct size, but its actual benefit in improving clinical outcomes remains to be established. In their excellent review article published recently in the Journal [1], Bulluck and Hausenloy describe elegantly the expectations emerged from the different forms of IC (pre-, per- and post- conditioning, applied locally or remotely). The authors present the clinical conditions where IC has been tested and they also provide novel thoughts regarding the potential to investigate its use in additional clinical settings. We fully agree that IC can be applied in percutaneous coronary intervention (PCI) during non-ST elevation myocardial infarction (NSTMI), as outlined in Figure 2, but not only in the form of remote ischaemic preconditioning (RIPC). Local ischemic postconditioning (IPost) has also been successfully applied in patients presented with non-totally occlusive coronary artery lesions; we have previously shown that IPost was feasible in patients with unstable angina and NSTMI and effective in reducing circulating biomarkers of oxidative stress, improving microcirculatory function in the short term as well as wall motion score index and left ventricular remodeling in the long term [2,3]. In addition, the authors report that the Hoole's study was the first one that tested the effect of limb remote ischaemic conditioning (RIC) in elective PCI. However, our group published the successful application of the intervention during elective PCI three years earlier, using actually a more potent RIC protocol with cuff inflation in both arms and at more appropriate timing [4]. Taking under consideration any piece of evidence derived by the available IC studies, even with opposing results, may enhance our efforts to recognize and overcome the obstacles that restrain the translation of the benefits demonstrated by proof-of-concept trials into the clinical setting.

    References 1. Bulluck H, Hausenloy DJ. Ischaemic conditioning: Are we there yet? Heart 2015;101:1067-77. 2. Iliodromitis EK, Paraskevaidis IA, Fountoulaki K, et al. Staccato reperfusion prevents reperfusion injury in patients undergoing coronary angioplasty: A 1-year follow-up pilot study. Atherosclerosis 2009;204:497 -502. 3. Ikonomidis I, Iliodromitis EK, Tzortzis S, et al. Staccato reperfusion improves myocardial microcirculatory function and long-term left ventricular remodeling: a randomized contrast echocardiography study. Heart 2010;96:1898-1903. 4. Iliodromitis EK, Kyrzopoulos S, Paraskevaidis IA, et al. Increased C reactive protein and cardiac enzyme levels after coronary stent implantation. Is there protection by remote ischaemic preconditioning? Heart 2006;92:1821-26.

    Conflict of Interest:

    None declared

    Read all letters published for this article

    Submit response
  6. Complete revascularization in STEMI

    Cover Letter

    Complete revascularization in STEMI

    a Ramez Nairooz, MD, b Srihari S Naidu, MD.

    a Division of Cardiology, University of Arkansas for Medical Sciences, Little Rock, Arkansas; b Division of Cardiology, Winthrop University Hospital, Mineola, New York.

    Funding: None Conflicts of interest: none Word Count: 325 Corresponding author & (address for reprints) Ramez Nairooz, MD Division of Cardiology University of Arkansas for Medical Sciences 4301 West Markham, Slot 532, Little Rock, AR 72205-7199 Tel: (714)-606-5550; Fax: (501)-686-6439 Email: ramez.nairooz@gmail.com

    Letter to editor

    We read with interest the recently published meta-analysis by Kowalewski and colleagues (1) titled "Complete revascularization in ST- elevation myocardial infarction and multivessel disease: meta-analysis of randomized controlled trials". However, we feel there are a few questions that need addressing: 1. The authors define complete revascularization as "revascularization to non-infarct-related artery lesions during index procedure" and non- complete MV-PCI "encompassed culprit only revascularization and staged approaches". Hence we ask the authors why they used the CvLPRIT (2) event numbers for the total population in whom complete revascularization was done both same setting and staged during index hospitalization? Shouldn't they have used the clinical outcomes of immediate vs staged PCI (published as supplementary material) to stay true to their definition?

    2. Is staged PCI during index hospitalization same as after discharge at later date revascularization? Can they be all added in one group "non- complete MV-PCI"? Maamoun et al scheduled the second procedure at 7 days, Ochala had the second procedure at average of 27 days while Politi et al staged it at an average of 56 days. How did staged PCI become bundled in the same group with infarct related artery only revascularization as seen in PRAMI, CvLPRIT and HELP-AMI? Thus we ask the authors were there any differences in outcomes of those who were staged in hospital vs staged at a later time?

    3. Finally we ask, what conclusion should clinicians draw from this analysis based on the heterogeneous trials which constitute it? Can clinicians conclude meaningful deductions regarding same setting complete revascularization (CR) vs index hospitalization CR vs later date CR vs infarct related artery only revascularization? These questions face the interventional community on daily basis and have no conclusive answer, with guidelines remaining equivocal on the topic. The COMPLETE trial (NCT01740479), currently ongoing, may shed some light on index hospitalization CR vs. infarct related artery only revascularization as the initial strategy, but cannot entirely answer the question as to optimal strategy.

    References: 1. Kowalewski M, Schulze V, Berti S, et al. Complete revascularisation in ST-elevation myocardial infarction and multivessel disease: meta-analysis of randomised controlled trials. Heart. 2015 Jun 2. pii:heartjnl-2014- 307293. doi: 10.1136/heartjnl-2014-307293. [Epub ahead of print] 2. Gershlick AH, Khan JN, Kelly DJ, et al. Randomized trial of complete versus lesion-only revascularization in patients undergoing primary percutaneous coronary intervention for STEMI and multivessel disease: the CvLPRIT trial. J Am Coll Cardiol. 2015;65:963-72.

    Conflict of Interest:

    None declared

    Read all letters published for this article

    Submit response
  7. The key role of the right ventricle in the pathogenesis of acute pulmonary oedema

    The article entitled "The pathophysiology of hypertensive acute heart failure"[1] provides a contemporary review of mechanisms involved in the development of acute pulmonary oedema (APO). We wish to highlight the potential key role of the right ventricle in the pathogenesis of APO.[2]

    APO is often thought to result from backward pressure where a disease of the left ventricle causes the left ventricular end-diastolic pressure to rise resulting in elevated pulmonary venous pressure and hence pulmonary capillary hydrostatic pressure. However, an increase in a given pressure can only occur if there is energy is either added or converted (eg kinetic to pressure energy). Since the conversion of kinetic energy to pressure energy is too small to result in a significant rise in pressure, the latter cannot be a dominant mechanism.

    We suggest that extra pressure energy is added by the right ventricle.[3] If the left ventricular stroke volume (LVSV) falls and the right ventricular stroke volume (RVSV) is unchanged, there are two effects: i) a beat by beat increase in the blood in the pulmonary circulation, and ii) a progressive rise in left ventricular diastolic pressure. The acute elevation of LVEDP must be a consequence of the increased energy added by RV rather than due to back pressure as a direct result of a LV disease.[2, 3]

    In situations of a high afterload the contractile stress required to maintain normal LVSV may be transiently exceeded. In the presence of a relatively normal RV, a mismatch between LV and RV stroke volumes results. An increased catecholamine drive causes augmented RV contractility and systemic venous constriction, stimulating the RV Frank Starling mechanism and increasing RVSV and pulmonary pressure. However, any disease of the left ventricle results in a failure to increase the left heart output even in the presence of adrenergic drive or LV Frank-Starling response.[4] There is inevitably a fluid shift from the systemic circulation to the pulmonary circulation and a rise in pulmonary artery pressure, capillary hydrostatic pressure, and consequently, LVEDP. Any evaluation of pathophysiology of APO that ignores the critical role of the right ventricle is incomplete.

    1 Viau DM, Sala-Mercado JA, Spranger MD, et al. The pathophysiology of hypertensive acute heart failure. Heart 2015.

    2 MacIver DH, Clark AL. The vital role of the right ventricle in the pathogenesis of acute pulmonary edema. The American journal of cardiology 2015;115:992-1000.

    3 MacIver DH, Dayer MJ, Harrison AJ. A general theory of acute and chronic heart failure. Int J Cardiol 2013;165:25-34.

    4 Kitzman DW, Higginbotham MB, Cobb FR, et al. Exercise intolerance in patients with heart failure and preserved left ventricular systolic function: failure of the Frank-Starling mechanism. J Am Coll Cardiol 1991;17:1065-72.

    Conflict of Interest:

    None declared

    Read all letters published for this article

    Submit response
  8. True and true, but not a paradox

    The journal, Heart, recently published a meta-analysis(1) and a commentary(2) on the association of obesity and mortality in patients with Coronary Heart Disease (CHD). Lavie begins his commentary with a story of two hypothetical patients with CHD. One has a BMI of 23 kg/m2 (normal) and the other has a BMI of 32 kg/m2 (obese).(2) Lavie asks about their prognosis. The meta-analysis by Wang et al(1) suggests that the obese patient has the better prognosis. Given that numerous primary prevention studies document that obesity is a cause of CHD, Lavie labels it a "paradox" that the prognosis would be better for the obese patient.

    It is true that obesity is a cause of CHD, and, as shown by Wang et al,(1) it is true that the obese people with CHD have a better prognosis than the non-obese people with CHD. However, this is not a paradox. The results are a function of the well-described phenomenon called, "collider stratification bias."(3) Consider that a person contracts CHD due to either (a) obesity or (b) factors unrelated to obesity (e.g. genetics or infectious diseases). If the causes unrelated to obesity are more strongly associated with the outcome of interest (i.e. mortality), then obesity appears protective. This is similar to analyses finding that maternal- smoking appears protective against infant mortality if one evaluates only low birth weight babies.(4)

    It is misleading to imply that obesity is protective in people with CHD. In the example by Lavie, the non-obese subject is not similar to the obese subject in ways other than obesity.(2) The non-obese subject with CHD must have contracted CHD from factors unrelated to obesity such as genetics or infectious disease. The apparent "obesity paradox" occurs because of confusion with the groups being compared. The comparison is not between obese people and non-obese people. Rather, the comparison is between people who have CHD presumably due to the ramifications of obesity and people who have CHD due to causes unrelated to obesity. The conclusion is not that obesity is protective, but rather that there are other causes of CHD that are more life-threatening than obesity.

    1. Wang ZJ, Zhou YJ, Galper BZ, Gao F, Yeh RW, Mauri L. Association of body mass index with mortality and cardiovascular events for patients with coronary artery disease: A systematic review and meta-analysis. Heart. 2015. doi: heartjnl-2014-307119. 2. Lavie CJ, De Schutter A, Milani RV. Body composition and the obesity paradox in coronary heart disease: Can heavier really be healthier? Heart. 2015. doi: heartjnl-2015-307966. 3. Banack HR, Kaufman JS. Does selection bias explain the obesity paradox among individuals with cardiovascular disease? Ann Epidemiol. 2015;25(5):342-349. 4. Hernandez-Diaz S, Schisterman EF, Hernan MA. The birth weight "paradox" uncovered? Am J Epidemiol. 2006;164(11):1115-1120.

    Conflict of Interest:

    None declared

    Read all letters published for this article

    Submit response
  9. Correspondence: A not so typical pericardial effusion case....

    To the Editor: We have read with interest the article of Miranda WR and coauthors1, in which a case of effusive-constrictive pericarditis is presented. This is a comprehensive and educational case that provides clinicians with a valuable message. Some points, however, require additional clarification in order to further strengthen the impact of this case. In particular, it is mentioned in the introduction that the patient was diagnosed with 'idiopathic pericarditis'. Nonetheless, the diagnosis of pericarditis is established in the presence of at least 2 out of the 4 main criteria including chest pain, pericardial friction, typical ECG changes and pericardial effusion.2 CRP elevation and pericardial inflammation in the cardiac magnetic resonance imaging (cMR) both constitute supportive findings. Accordingly, since only one diagnostic criterion was fulfilled (i.e. pericardial effusion), it should probably be more appropriate to 'label' the patient's disorder as 'idiopathic pericardial effusion' rather than 'idiopathic pericarditis'. Concerning treatment, the patient received initially colchicine as an outpatient, despite normal baseline CRP values. However, in the absence increased CRP levels, the efficacy of colchicine is questionable in chronic idiopathic pericardial effusion.3 Furthermore, even in the setting of idiopathic pericarditis, which this patient was presumed to have, colchicine is beneficial when administered in conjunction with either aspirin/non-steroidal anti-inflammatory (NSAID) medications or corticosteroids, but not as monotherapy.3 Another intriguing finding in this case was the demonstration of active pericardial inflammation in cMR. This is a quite unexpected finding in the presence of normal baseline CRP levels. Since pericardiocentesis and drainage catheters are potential triggers of pericardial inflammation, one wonders if pericardiocentesis was the actual cause of pericardial inflammation. Along this line, it would be interesting to know the post- pericardiocentesis serum CRP levels. Last but not least, the patient became asymptomatic and the jugular pressure normalized within 72 hours after aggressive NSAID therapy. This turn of events strongly suggests transient pericardial constriction, namely a reversible cause of pericardial constriction, which is occasionally observed towards the end of the effusive period of pericarditis.4 In conclusion, a final diagnosis of idiopathic pericardial effusion (possibly post-pericarditis) with transitory constriction probably unifies all aspects of this challenging case.

    References 1 Miranda WR, Newman DB, Nishimura RA. A not so typical pericardial effusion case....Heart 2015 Jun 17. pii: heartjnl-2015-308115. 2 Imazio M, Gaita F. Diagnosis and treatment of pericarditis. Heart 2015 Apr 8. pii: heartjnl-2014-306362. 3 Brucato A, Brambilla A, Adler Y, Spodick,D. Colchicine for Recurrent Acute Pericarditis. Arch Intern Med 2006;166:696. 4 Haley JH, Tajik AJ, Danielson GK, et al. Transient constrictive pericarditis: causes and natural history. J Am Coll Cardiol 2004;43:271-5.

    Conflict of Interest:

    None declared

    Read all letters published for this article

    Submit response
  10. Importance of the UK health care model for success in cardiovascular disease control compared the health care model in Turkey

    We read the paper of Bhatnagar P. et al. 1 and were impressed by great success of the UK health care on control of cardiovascular disease (CVD). In the UK during last decade, CVD decreased from top to 2nd row on mortality of men in whom, lipid lowering drugs were the most prescribed medicine. 1 In this report, importance of primary care and increased number of less invasive approaches like angioplasty compared to surgery were pointed out. We compared some data here with performance-based procedure-dependent income model for physicians in Turkey during the last decade. All individuals can apply to a tertiary hospital since absence of compulsory referral system in this model.

    Decreased number of referred patients may not eliminate low risk group and high risk patients may not be treated effectively, then more severely ill patients may be detected in a vicious circle. Since the health autority has started to act in 2002, the number of refered patients from primary care has decreased and operations has increased from 22 %, 1.598.362 to 3 %, 4.684.237 respectively in 2013. 2 Nevertheless, CVD continues to be the biggest killer in Turkey. In this model, increased applications may be seen as a profitable investment. In fact, the total number of private hospitals has gradually increased from 271 in 2002 and to 550 in 2013 in Turkey. 2 Interestingly, instead of encouraging preventive approach, it was tried to settle a mandatory on call arrangement for primary care physicians differently from UK. Fortunately, that was blocked by social consciousness.

    Limited time for diagnostic tests in Turkish model may be a disadvantage for prevention of organ damage in hypertension. One of five patients with previously undiagnosed hypertension, the leading risk for CVD is associated with subclinical target organ damage including cardiac remodelling. 3 Early determination of cardiac remodelling and exercise hypertension have gained more importance, 4 however, they may be ignored in clinical practice. Exercise hypertension may be missed even in large national registiries, therefore, we recently have mentioned its importance in healthy individuals who develope early cardiac remodelling in British registry (LARGE). 4

    1. Bhatnagar P, Wickramasinghe K, Williams J, et al. The epidemiology of cardiovascular disease in the UK 2014. Heart 2015;0:1-8. doi:10.1136/heartjnl-2015-307516. 2. Kose MR, Basara BB, Guler C, Yentur GK. Turkish Republic, Ministry of Health. Annual Health Statistics, Ankara, 2013. 3. Korhonen PE, Kautiainen H, Jarvenpaa S, Kantola I. Target organ damage and cardiovascular risk factors among subjects with previously undiagnosed hypertension. Eur J Prev Cardiol 2013; 21:980-8. 4. Yalcin F, Abraham TP, Gottdiener JS. Letter regarding the article by Lee PT, et al. Left ventricular wall thickness and the presence of asymmetric hypertrophy in healthy young army recruits: data from the LARGE heart study. Circ Cardiovasc Imaging 2013;6:e28.

    Conflict of Interest:

    None declared

    Read all letters published for this article

    Submit response

Free sample
This recent issue is free to all users to allow everyone the opportunity to see the full scope and typical content of Heart.
View free sample issue >>

Don't forget to sign up for content alerts so you keep up to date with all the articles as they are published.