Form Dl 62 2007: Fill & Download for Free

Most fifties (Overall)Player Span Mat Inns NO Runs HS Ave 100 50 50+ 0SR Tendulkar (INDIA) 1989-2013 664 782 74 34357 248* 48.52 100 164 264 34RT Ponting (AUS/ICC) 1995-2012 560 668 70 27483 257 45.95 71 146 217 39KC Sangakkara (Asia/ICC/SL) 2000-2015 594 666 67 28016 319 46.77 63 153 216 28JH Kallis (Afr/ICC/SA) 1995-2014 519 617 97 25534 224 49.10 62 149 211 33R Dravid (Asia/ICC/INDIA) 1996-2012 509 605 72 24208 270 45.41 48 146 194 21DPMD Jayawardene (Asia/SL) 1997-2015 652 725 62 25957 374 39.15 54 136 190 47S Chanderpaul (WI) 1994-2015 454 553 94 20988 203* 45.72 41 125 166 21BC Lara (ICC/WI) 1990-2007 430 521 38 22358 400* 46.28 53 111 164 33Inzamam-ul-Haq (Asia/ICC/PAK) 1991-2007 499 551 76 20580 329 43.32 35 129 164 35SC Ganguly (Asia/INDIA) 1992-2008 424 488 40 18575 239 41.46 38 107 145 29ST Jayasuriya (Asia/SL) 1989-2011 586 651 35 21032 340 34.14 42 103 145 53AB de Villiers (Afr/SA) 2004-2016 383 441 60 18184 278* 47.72 45 95 140 18Mohammad Yousuf (Asia/PAK) 1998-2010 381 432 52 17300 223 45.52 39 97 136 26CH Gayle (ICC/WI) 1999-2016 422 493 32 17954 333 38.94 39 97 136 40ME Waugh (AUS) 1988-2002 372 445 37 16529 173 40.51 38 97 135 35AR Border (AUS) 1978-1994 429 517 83 17698 205 40.77 30 102 132 22DL Haynes (WI) 1978-1994 354 439 53 16135 184 41.80 35 96 131 23SR Waugh (AUS) 1985-2004 493 548 104 18496 200 41.65 35 95 130 37GC Smith (Afr/ICC/SA) 2002-2014 347 432 25 17236 277 42.34 37 90 127 20IVA Richards (WI) 1974-1991 308 349 36 15261 291 48.75 35 90 125 17Javed Miandad (PAK) 1975-1996 357 407 62 16213 280* 46.99 31 93 124 14MJ Clarke (AUS) 2003-2015 394 449 71 17112 329* 45.26 36 86 122 21TM Dilshan (SL) 1999-2016 497 527 64 17671 193 38.16 39 83 122 35Younis Khan (PAK) 2000-2016 402 479 44 17370 313 39.93 40 81 121 41PA de Silva (SL) 1984-2003 401 455 41 15645 267 37.78 31 86 117 24HM Amla (SA) 2004-2016 274 338 28 15095 311* 48.69 48 66 114 13AC Gilchrist (AUS/ICC) 1996-2008 396 429 32 15461 204* 38.94 33 81 114 33G Kirsten (SA) 1993-2004 286 361 34 14087 275 43.07 34 79 113 24SP Fleming (ICC/NZ) 1994-2008 396 463 31 15319 274* 35.46 17 95 112 33V Sehwag (Asia/ICC/INDIA) 1999-2013 374 443 15 17253 319 40.31 38 72 110 31ML Hayden (AUS/ICC) 1993-2009 273 348 32 15066 380 47.67 40 69 109 23MS Dhoni (Asia/INDIA) 2004-2016 446 453 115 15098 224 44.66 15 94 109 19V Kohli (INDIA) 2008-2016 272 297 43 13186 211 51.91 40 68 108 14IR Bell (ENG) 2004-2015 287 370 39 13331 235 40.27 26 82 108 20M Azharuddin (INDIA) 1984-2000 433 455 63 15593 199 39.77 29 79 108 14SM Gavaskar (INDIA) 1971-1987 233 316 30 13214 236* 46.20 35 72 107 20AN Cook (ENG) 2006-2016 234 345 19 14199 294 43.55 35 72 107 15MS Atapattu (SL) 1990-2007 360 416 47 14036 249 38.03 27 76 103 35HH Gibbs (SA) 1996-2010 361 417 24 14661 228 37.30 35 66 101 37Saeed Anwar (PAK) 1989-2003 302 335 21 12876 194 41.00 31 68 99 23KP Pietersen (ENG/ICC) 2004-2014 277 342 29 13797 227 44.07 32 67 99 18A Flower (ZIM) 1992-2003 276 320 35 11580 232* 40.63 16 82 98 18GA Gooch (ENG) 1975-1995 243 337 12 13190 333 40.58 28 69 97 17Saleem Malik (PAK) 1982-1999 386 410 60 12938 237 36.96 20 76 96 31CG Greenidge (WI) 1974-1991 236 312 29 12692 226 44.84 30 65 95 14DC Boon (AUS) 1984-1996 288 367 36 13386 200 40.44 26 69 95 22A Ranatunga (SL) 1982-2000 362 410 59 12561 135* 35.78 8 87 95 30BB McCullum (NZ) 2002-2016 432 474 47 14676 302 34.37 19 76 95 37MEK Hussey (AUS) 2004-2013 302 324 71 12398 195 49.00 22 72 94 16LRPL Taylor (NZ) 2006-2016 327 369 57 12920 290 41.41 31 62 93 25NJ Astle (NZ) 1995-2007 308 358 25 11866 222 35.63 27 65 92 30RB Richardson (WI) 1983-1996 310 363 42 12197 194 37.99 21 71 92 16AJ Stewart (ENG) 1989-2003 303 397 35 13140 190 36.29 19 73 92 27Misbah-ul-Haq (PAK) 2001-2016 270 303 62 10785 161* 44.75 10 81 91 15RR Sarwan (WI) 2000-2013 286 339 44 11944 291 40.48 20 71 91 21VVS Laxman (INDIA) 1996-2012 220 308 41 11119 281 41.64 23 66 89 17MA Taylor (AUS) 1989-1999 217 296 14 11039 334* 39.14 20 68 88 9Yuvraj Singh (Asia/INDIA) 2000-2016 388 378 54 11363 169 35.07 16 70 86 26G Gambhir (INDIA) 2003-2016 242 283 18 10324 206 38.95 20 63 83 20AJ Strauss (ENG) 2003-2012 231 308 14 11315 177 38.48 27 54 81 25SR Watson (AUS) 2002-2016 307 334 36 10950 185* 36.74 14 67 81 21Updated till dec 9, 2016.

No.The reason is that high cholesterol is not the main risk factor for cardiovascular disease (CVD). According to WHO (2011) are the risk factors the following:And in 2018 did WHO add hydrogenated trans fats to the list: WHO plan to eliminate industrially-produced trans-fatty acids from global food supply.Yes.Some people have high cholesterol due to a gene defect. This is called familial hypercholesterolemia. It is a common belief that this increases the risk for CVD. But not everyone agrees.Have you heard about The Framingham Heart Study?The Framingham Heart Study in Massachusetts, USA, has been running continuously since 1948. The study began with 5,209 inhabitants in Framingham aged between 30 and 62, and with no history of heart disease or stroke. The study is now on its third generation of participants.The objective of the Framingham Heart Study was to identify the common factors or characteristics that contribute to CVD by following its development over a long period of time in a large group of participants who had not yet developed overt symptoms of CVD or suffered a heart attack or stroke.The study has lead to the identification of the major CVD risk factors as well as a great deal of valuable information on the effects of related factors such as blood triglyceride and HDL cholesterol levels, age, gender, and psychosocial issues.In march 1971, this graph was published in Human Pathology - Volume 2, Number 1:Average cholesterol levels was 220 mg/dl.Half of the group that did not develop CHD had higher cholesterol levels.Half of the group that developed CHD had lower cholesterol levels, albeit there is an increase around 300 mg/dl.LDL particles (LDL-P) appear in different sizes:Large LDL particles are called "Pattern A". They are fluffy in substance and can carry large amounts of cholesterol. Therefore is the number of LDL particles low.Small LDL particles are called "Pattern B". They are dense and can only carry small amounts of cholesterol. Therefore is the number of LDL particles high.In 2007 was it published a study in NCBI named "LDL Particle Number and Risk of Future Cardiovascular Disease in the Framingham Offspring Study – Implications for LDL Management".This study ran for nearly 16 years, and the participants were divided into four groups with high and low LDL-C and high and low LDL-P respectively. ​The study shows that those with high LDL-P have higher risk for cardiovascular disease than those with low LDL-P, regardless of their LDL-C.

Aspirin is a so-called antiplatelet drug. It prevents the formation of blood clots by reducing the reactivity of platelets, that is their tendency to aggregate. This only works in the prevention of ischaemic events which happen due to rupture of an atheromatous plaque or due to critical narrowing of an artery, but not due to thromboembolic events, whereby a blood clot forms in a vein or the heart and then embolises into an artery of the heart or the brain, as is the case with thromboembolic events (typically stroke) in atrial fibrillation or patent foramen ovale.The pathophysiology of a blood clot forming in a vessel or heart chamber with low blood velocity (as is the case with blood clots in the veins and the atria of the heart) is a different one than the pathophysiology of a blood clot forming in an environment of high blood velocity, such as along the artery walls (where an antiplatelet drug would suffice). For the prevention of thromboembolic events one needs drugs which inhibit the coagulation cascade that happens after the initial platelet aggregation, so called anticoagulants (such as heparin, warfarin or the new oral anticoagulants, such as rivaroxaban, dabigatran, apixaban or edoxaban).Now that we have established that aspirin only helps prevent ischaemic events which happen due to atherosclerosis and not due to thromboembolism, let’s also get another thing out of the way:In medicine, there are two types of prevention: primary and secondary prevention. Primary prevention refers to individuals with risk factors for an (in this case ischaemic) event who have not manifested the disease yet (be it coronary artery disease or cerebrovascular disease). Secondary prevention refers to individuals who have already had one ischaemic event.There are numerous studies which have shown that aspirin is quite successful in the secondary prevention of ischaemic events both in men and in women. So, if anyone is reading this who has ever had an ischaemic attack (heart attack or stroke) or who has received a stent due to critical narrowing of a artery, rest assured that you need some type of medication which makes the blood clot less (whether aspirin or another drug or aspirin plus another drug, your doctor will have told you). The studies are too numerous to include here, I will include just one, which showed that aspirin can be combined with a low dose anticoagulant in order to further improve secondary prevention, both in men and in women:Rivaroxaban with or without Aspirin in Stable Cardiovascular Disease | NEJMNow coming to the difficult part, primary prevention. One would instinctively believe that aspirin should be able to also prevent primary events if it can prevent secondary events. If it works for patients with advanced atherosclerosis, why shouldn’t it be able to prevent events in people with significant risk factors for atherosclerosis who have not yet had an event?Various meta-analyses of studies performed in the last decades have shown that aspirin use in primary prevention is supposed to reduce the risk of myocardial infarction in men and the risk of ischaemic stroke in women, but not the other way round (whereby one must point out that the results about the prevention of stroke in women were pulled mainly by a single large study). Remember also, there is haemorrhagic stroke too, which is caused by bleeding in the brain, so aspirin should decrease the risk for ischaemic stroke to a considerably greater effect than it might increase the risk for haemorrhagic stroke so as to be beneficial in primary prevention.According to a meta-analysis published in PLoS One in 2014, Aspirin for Primary Prevention of Cardiovascular Events: Meta-Analysis of Randomized Controlled Trials and Subgroup Analysis by Sex and Diabetes Status, the number of people that one would need to treat with aspirin in order to prevent the first occurrence of 1 major cardiovascular event over a mean follow-up of 6.8 years was 284. By comparison, the number of people than one would treat until one saw 1 major bleeding (number needed to harm) was 299. In subgroup analyses, pooled results demonstrated a reduction in myocardial infarction among men (0.71; 0.59–0.85) and ischaemic stroke among women (0.77; 0.63–0.93).Why there is this gender difference, if there really is one, one can only speculate:The different epidemiologic characteristics of cardiovascular disease between men and women may contribute to the different benefits. After age 40 years, men have a 49% lifetime risk for a coronary heart disease event, while women have a 32% risk. On the other hand, the lifetime risk for ischaemic stroke is greater in women (17–18%) than men (13–14%) from age 55 to 75, because women tend to live longer, long enough to experience a stroke. If aspirin only has a modest protective effect, the effect is more likely to show for the most common kind of ischaemic event for each gender.The two genders might differ in their platelet’s sensitivity to aspirin(there are conflicting studies about whether there is an aspirin “resistance” and whether women’s platelets have a higher reactivity compared to their male counterparts).Men and women may differ in their compliance concerning the aspirin therapy. If coronary artery disease produces more atypical symptoms in women than in men, women might not be as alert as men in re-introducing the aspirin when the disease begins to manifest itself (although in this case we should not be talking of primary prevention anymore).One should not forget that aspirin is not the only tool for the prevention of cardiovascular disease. There are other tools in the arsenal, both for men and for women (see Comprehensive primary prevention of cardiovascular disease in women).Since its 2016 statement (Aspirin Use for the Primary Prevention of Cardiovascular Disease and Colorectal Cancer: U.S. Preventive Services Task Force Recommendation Statement), the U.S. Preventive Services Task Force has been recommending low-dose aspirin for the primary prevention of cardiovascular disease (and colorectal cancer!) in adults aged 50 to 59 years who have a 10% or greater 10-year risk of cardiovascular disease, are not at increased risk for bleeding, have a life expectancy of at least 10 years, and are willing to take low-dose aspirin daily for at least 10 years, whereas the decision for adults aged 60 to 69 should be an individual one. For adults younger than 50 or older than 70, the evidence was found to be insufficient.But how to determine who has a 10% or greater risk of developing cardiovascular disease in the next 10 years? Sure, there are scores, established years ago. But therein lies the problem with today’s primary prevention: The general population at risk of cardiovascular disease is nowadays becoming “ever more healthy”, as risk factors such as arterial hypertension and hyperlipidaemia are better controlled with ever more effective drugs (see statins), for modest aspirin to show any effect at all.So,after the (long) prologue, may I present to you the results of the latest randomised, double-blind, placebo-controlled trial, the ARRIVE trial, published in August 2018 in The Lancet,Use of aspirin to reduce risk of initial vascular events in patients at moderate risk of cardiovascular disease (ARRIVE): a randomised, double-blin... - PubMed - NCBI,which addressed the question of the role of aspirin in the prevention of ischaemic events in patients at moderate risk for cardiovascular disease (defined as a 10–20% risk to develop coronary artery disease within the next 10 years or else a 20–30% risk to develop any cardiovascular disease within the next 10 years), with the exclusion of patients with diabetes (more about that later).Between July 2007 and Nov 2016, 12 546 patients were enrolled and randomly assigned to receive aspirin (n=6270, of which 1851 were women) or placebo (n=6276, of which 1857 were women) at 501 study sites. Women made up 29·6% of the patients, equally distributed between the aspirin and the control group. Median follow-up was 60 months.Eligible male patients were aged 55 years and older and had between two and four risk factors. Eligible female patients were aged 60 years or older and had three or more risk factors. Risk factors were:high cholesterol (total cholesterol > 240 mg/dL [6·126 mmol/L] or LDL > 160 mg/dL [4·144 mmol/L] for women) irrespective of current treatmentlow HDL cholesterol (< 40 mg/dL)current smokinghigh blood pressure (systolic blood pressure >140 mm Hg) or receiving medication to treat high blood pressurea positive family history of cardiovascular heart disease.The eligibility criteria were based on various European and US risk calculators. Patients were excluded if they had a history of a vascular event (such as stroke or a myocardial infarction), congestive heart failure, relevant arrhythmias, coronary artery bypass graft, coronary artery angioplasty or stenting or any other vascular intervention. Patients were also ineligible if they already required antiplatelet therapy, if they were at high risk of gastrointestinal and other bleeding (such as when they had a history of such a bleeding or of gastric or duodenal ulcers) as well as those requiring concomitant use of anticoagulants or frequent use of NSAIDs.As mentioned before, patients with diabetes were also excluded due to their higher risk and the fact that there was already another study underway examining aspirin’s effect on diabetics. In fact, a meta-analysis has found no clear benefit from aspirin in diabetic patients despite their higher cardiovascular risk (Aspirin for primary prevention of cardiovascular and all-cause mortality events in diabetes: updated meta-analysis of randomized controlled trials).Coming back to the ARRIVE trial in non-diabetics, the primary efficacy endpointwas a composite outcome consisting of time to first occurrence of:confirmed myocardial infarction (MI)strokecardiovascular deathunstable angina (UA) ortransient ischaemic attack (of the brain) (TIA)The last two were added later on by protocol amendments because of the low event rate and because patients in the control group who experienced either UA or TIA had to start taking aspirin anyway.What did the study find out?Because of this and that (explained below), the patients who were actually treated (and thus analysed) according to the protocol were 3790 (60·4%) in the aspirin group and 3912 (62·3%) in the control group.If we go by the intention-to-treat analysis, looking at the events for all the patients in the aspirin and the control group irrespective of their compliance, we get absolutely no benefit from aspirin, neither for the prevention of myocardial infarction nor for the prevention of stroke. The only difference between the two groups is that those in the aspirin group had significantly higher chance of gastrointestinal bleeding.Subgroup analyses according to the various patient characteristics (one of them being gender) were only performed concerning the composite endpoint (time to first occurrence of any cardiovascular event), as to which both men and women were equal, irrespective of whether they were in the aspirin or in the control group. There was no information on whether men and women differed in the incidence of myocardial infarctions and unstable angina versus stroke and transient ischaemic attacks.If we go by the per-protocol analysis, looking at only the 60·4% in the aspirin group and the 62·3% in the control group who were treated and analysed according to protocol, we see a benefit from aspirin concerning the incidence of myocardial infarctions (and again, more cases of gastrointestinal bleeding on aspirin). There was no information on subgroup analysis according to patient characteristics, so we do not know how men and women did comparatively to each other.(I am sorry for the bad quality of the pdf snapshot, as I had to scan it from the appendix:)What does our study teach us about the use of aspirin in the primary prevention for patients in moderate risk for cardiovascular disease?As the investigators say, nothing.Firstly, the study was supposed to be done on people with a moderate cardiovascular risk, but ended up investigating a low risk populationinstead. The actual cardiovascular event rate in each group, transformed to a 10-year rate, was considerably lower than the expected (8·43% instead of 11·4% in the aspirin group, 8·8% instead of 13·4% for the placebo group, whereas the expected 13·4% were already lower than the initially expected 17·3% before enrolment started).Remember that the U.S. Preventive Services Task Force recommends aspirin for primary prevention when the 10-year risk for cardiovascular disease is moderate (10–20%) or higher, so 10% can be thought of as a cut-off, below which aspirin has little to no positive effect compared to the increased risk of bleeding.43% of the participants in the ARRIVE study were taking a statin for high cholesterol, which may have lowered their cardiovascular risk significantly. Whether a participant was taking a statin or not did not seem to have an influence on whether aspirin would prevent a cardiovascular event (in both cases it didn’t), but one may assume that those without a statin had a lower baseline cholesterol, hence a lower cardiovascular risk anyway.Secondly, the interpretation of the results is difficult because of the relatively poor adherence to protocol. Approximately 29·7% patients discontinued their participation in the study (with an almost equal percentage of discontinuation on both the aspirin and the placebo arm), mainly due to withdrawal of their consent. Of the remaining patients, 637 (10·2%) in the aspirin group did not take aspirin compliantly for more than 60% of the time, whereas 472 (7·5%) in the placebo group started taking aspirin at some point despite not having had an ischaemic event which would have required them to do so.A large portion of the incompliant patients as well as the patients who withdrew from the study was from the UK, where a public discussion was going on about the uncertainty of the benefits and dangers of the use of aspirin in primary prevention.Are we back to point zero?I don’t think so. The study has taught us that the risk calculators both of the American Heart Association as well as the European Society of Cardiology need to be readjusted in the statin era, so as to better reflect the overall improvement of the cardiovascular risk of the general population who is under statin treatment. Then, the question about who needs aspirin needs to be re-addressed, this time on patients with a higher event rate and a better compliance, preferably with a predetermined subgroup analysis according to gender, age and intensity of statin treatment.Bottom-line is, if your doctor tells you to take an aspirin and you have no known cardiovascular disease, you should ask your doctor whether he has estimated your 10-year cardiovascular risk yet before prescribing the aspirin (I don’t mean the calculation with the risk scores of the various Cardiology societies that you can find online such as the ACC/AHA ASCVD Risk Calculator, the ESC’s HeartScore or the Framingham Coronary Heart Disease Risk Score, because they do not necessarily reflect your individual risk correctly. I mean an estimation of your individual 10-year cardiovascular risk based on the integration of all the information that your doctor has about you and the relevant circumstances of your life, past, present and future.) If he has and you are above 10% and have no history of gastrointestinal bleeding, you would be advised to take it.