Framingham Risk Score Calculator Pdf' title='Framingham Risk Score Calculator Pdf' />The Framingham Risk Score is a genderspecific algorithm used to estimate the 10year cardiovascular risk of an individual. The Framingham Risk Score was first. The straight dope on cholesterol Part VII Previously, in Part I, Part II, Part III, Part IV, Part V ,and Part VI of this series, we addressed these 8 concepts     1 What is cholesterol     2 What is the relationship between the cholesterol we eat and the cholesterol in our body     3 Is cholesterol bad     4 How does cholesterol move around our body     5 How do we measure cholesterol     6 How does cholesterol actually cause problems     7 Does the size of an LDL particle matter     8 Why is it necessary to measure LDL P, instead of just LDL C In this post well continue to build out the story with the next concept     9 Does HDL matter after allNo so Quick refresher on take away points from previous posts, should you need it Cholesterol is just another fancy organic molecule in our body but with an interesting distinction we eat it, we make it, we store it, and we excrete it all in different amounts. The pool of cholesterol in our body is essential for life. No cholesterol no life. Cholesterol exists in 2 forms unesterified or free UC and esterified CE and the form determines if we can absorb it or not, or store it or not among other things. Much of the cholesterol we eat is in the form of CE. It is not absorbed and is excreted by our gut i. The reason this occurs is that CE not only has to be de esterified, but it competes for absorption with the vastly larger amounts of UC supplied by the biliary route. Re absorption of the cholesterol we synthesize in our body i. That is, most of the cholesterol in our body was made by our body. The process of regulating cholesterol is very complex and multifaceted with multiple layers of control. Ive only touched on the absorption side, but the synthesis side is also complex and highly regulated. You will discover that synthesis and absorption are very interrelated. Eating cholesterol has very little impact on the cholesterol levels in your body. This is a fact, not my opinion. Anyone who tells you different is, at best, ignorant of this topic. At worst, they are a deliberate charlatan. Years ago the Canadian Guidelines removed the limitation of dietary cholesterol. The rest of the world, especially the United States, needs to catch up. To see an important reference on this topic, please look here. Cholesterol and triglycerides are not soluble in plasma i. To be carried anywhere in our body, say from your liver to your coronary artery, they need to be carried by a special protein wrapped transport vessel called a lipoprotein. As these ships called lipoproteins leave the liver they undergo a process of maturation where they shed much of their triglyceride cargo in the form of free fatty acid, and doing so makes them smaller and richer in cholesterol. Special proteins, apoproteins, play an important role in moving lipoproteins around the body and facilitating their interactions with other cells. The most important of these are the apo. B class, residing on VLDL, IDL, and LDL particles, and the apo. A I class, residing for the most part on the HDL particles. Cholesterol transport in plasma occurs in both directions, from the liver and small intestine towards the periphery and back to the liver and small intestine the gut. The major function of the apo. B containing particles is to traffic energy triglycerides to muscles and phospholipids to all cells. Their cholesterol is trafficked back to the liver. Framingham-risk-score-Relation-to-5-year-risk-of-stroke-death-002959-408x306px.png' alt='Framingham Risk Score Calculator Pdf' title='Framingham Risk Score Calculator Pdf' />The apo. A I containing particles traffic cholesterol to steroidogenic tissues, adipocytes a storage organ for cholesterol ester and ultimately back to the liver, gut, or steroidogenic tissue. All lipoproteins are part of the human lipid transportation system and work harmoniously together to efficiently traffic lipids. Pharmacologic treatment of hyperlipidemia in conjunction with therapeutic lifestyle changes can be used for both primary and secondary prevention of cardiovascular. Number 0228. Policy. Rita Redshoes Golden Era there. Aetna considers cardiac computed tomography CT angiography of the coronary arteries using 64slice or greater medically necessary for the. As you are probably starting to appreciate, the trafficking pattern is highly complex and the lipoproteins constantly exchange their core and surface lipids. The measurement of cholesterol has undergone a dramatic evolution over the past 7. Currently, most people in the United States and the world for that matter undergo a standard lipid panel, which only directly measures TC, TG, and HDL C. LDL C is measured or most often estimated. More advanced cholesterol measuring tests do exist to directly measure LDL C though none are standardized, along with the cholesterol content of other lipoproteins e. VLDL, IDL or lipoprotein subparticles. The most frequently used and guideline recommended test that can count the number of LDL particles is either apolipoprotein B or LDL P NMR, which is part of the NMR Lipo. Profile.   NMR can also measure the size of LDL and other lipoprotein particles, which is valuable for predicting insulin resistance in drug nave patients, before changes are noted in glucose or insulin levels. The progression from a completely normal artery to a clogged or atherosclerotic one follows a very clear path an apo. B containing particle gets past the endothelial layer into the subendothelial space, the particle and its cholesterol content is retained, immune cells arrive, an inflammatory response ensues fixing the apo. B containing particles in place AND making more space for more of them. While inflammation plays a key role in this process, its the penetration of the endothelium and retention within the endothelium that drive the process. The most common apo. B containing lipoprotein in this process is certainly the LDL particle. However, Lpa and apo. B containing lipoproteins play a role also, especially in the insulin resistant person. If you want to stop atherosclerosis, you must lower the LDL particle number. Period. At first glance it would seem that patients with smaller LDL particles are at greater risk for atherosclerosis than patients with large LDL particles, all things equal. A particle is a particle is a particle. If you dont know the number, you dont know the risk. With respect to laboratory medicine, two markers that have a high correlation with a given outcome are concordant they equally predict the same outcome. However, when the two tests do not correlate with each other they are said to be discordant. LDL P or apo. B is the best predictor of adverse cardiac events, which has been documented repeatedly in every major cardiovascular risk study. LDL C is only a good predictor of adverse cardiac events when it is concordant with LDL P otherwise it is a poor predictor of risk. There is no way of determining which individual patient may have discordant LDL C and LDL P without measuring both markers. Discordance between LDL C and LDL P is even greater in populations with metabolic syndrome, including patients with diabetes. Given the ubiquity of these conditions in the U. S. population, and the special risk such patients carry for cardiovascular disease, it is difficult to justify use of LDL C, HDL C, and TG alone for risk stratification in all but the most select patients. To address this question, however, one must look at changes in cardiovascular events or direct markers of atherosclerosis e. IMT while holding LDL P constant and then again holding LDL size constant. Only when you do this can you see that the relationship between size and event vanishes. The only thing that matters is the number of LDL particles large, small, or mixed. Concept 9 Does HDL matter after allCVDCHD Risk. Check. Pldoyer fr ein einheitliches Raster bei der Darstellung von Studien Resultaten. PV Prvalenz, Postvalenz, Inzidenz, Risiko gemeint ist die prozentuale Hufigkeit der Zielkrankheit in einer Untersuchungsgruppe Plazebo,Verum. PV Plazebo entspircht im B A Y E S Theorem den Krankheitswahrscheinlichkeiten PV bzw. PDW vor bzw. nach einem pos. Diagnose Test. NNT Number Needed to Treat ist die notwendige Anzahl zu behandelnden Patienten, um bei 1 Patienten eine erfolgreiche Behandlung der Zielkrankheit zur erreichen, ist ein Mass fr die richtige Allokation zielgerichtete Indikation, effizienter Mitteleinsatz. ARR Absolute Risiko. Reduktion, ist die reziproke NNT und umgekehrt. R I S K Rechner RRR Relative Risiko. Reduktion, ist ein Mass fr die Wirksamkeit einer therapeutischen Intervention, unabhngig von der richtigen Allokation. SLZ J Studienlaufzeit Jahre, ist der Divisor zur Berechnung der Jhrlichen Inzidenz zwecks Herstellung einer Vergleichbarkeit zwischen den diversen Studien. Die Acronyme stehen fr folgende Studien Quelle Whats What, Acronymguide for cardiovascular trials, Astra Hssle AB, Sweden. HHS Helsinki Heart Study, 1. Gemfibrozil Gevilon, 6. SLZ 5 Jahre. AFCAPS Air ForceTexas Coronary Atheosclerosis Prevention Study Lovastatin 2. SLZ 5. 2 Jahre. WOSCOPS West Of Scotland COronary Prevention Study, 1. Pravastatin 4. 0mg abends, SLZ 5 Jahre. CARE Cholesterol And Recurrent Events trial ongoing 5 J SLZ Pravastatin nach AMI, 4. RRR gegenber Placebo 2. CABG, 2. 3 in PTCA Gruppe. LIPID Long term Intervention with Pravastatin in Ischemic Disease Pravastatin Selipran 4. SLZ mean 6. 1 Jahre. VA HIT Veterans Affairs High density lipoprotein cholesterol Intervention Trial Gemfirbrozil Gevilon SR 1. SLZ median 5. 1 Jahre, 1. Placebo Inzidenz CHK Events. S Scandinavian Simvastatin Survival Study Simvastatin Zocor 2. SLZ median 5. 4 Jahre, 1. Placebo Inzidenz CHK Events. HPS Heart Protection Study Lancet,6. Simvastatin 4. 0mgdie, SLZ 5 Jahre, 2. Inzidenz major vascular events Herz,Cerebrum. Anmerkung 2. 1. 82. Lancet Original aufgefhrt rechnen die Angelsachsen anders Warum wohl hat das Paradebeispiel einer hchst effizienten Pharmakotherapie, nmlich die Lokalansthesie einer Region von 0. Krperoberflche eine NNT von 1 Die WZW Regel ist nicht eine Erfindung des unglckseligen KVG 1. Grundprinzip der rationalen Pharmakotherapie sparsamer, zielgerichteter richtige Allokation richtige Indikation, bedarfsgerechter bzw. Einsatz eines wirksamen Mittels in richtiger Dosis nach dem Motto zuviel am falschen Ort bringt nur Nebenwirkungen Die moderne Polypragmasie bzw. Polypharmacie eine rationale Pharmakotherapie Krankheiten, deren eigentliche Ursache sofern es eine solche berhaupt gibt man nicht kennt, behandelt man effizient nicht durch die maximale Beeinflussung eines einzelnen Risikofaktors sondern durch eine optimale Einflussnahme auf gleichzeitig mehrere Risikofaktoren Die therapeutischen Grenzen werden dabei gesetzt durch die hohen Anforderungen an die Patienten Compliance Therapieadhrenz,Therapietreue und die AM Nebenwirkungen Interaktionen. Die schwierige rztliche Kunst des Grundversorgers besteht in der Umsetzung der epidemilogischen Erkenntnisse in eine patientenadaptierte Individual Therapie. Der Wunsch eines Grundversorgers an die Grundlagenforschung bezglich der Umschreibung des CHK Risikos Fortentwicklung der derzeitigen Testbatterie Stufendiagnostik sensitivittslastige Screeningmethoden gefolgt von spezifittslastigen Diagnosemethoden mit dem Ziel einer p. PDW fr AMI 0. 0. Jahr kumuliert in 1. Jahren auf 0. 8 8. Qualitts Anforderungen an eine solche Diagnosemethode Arteriosklerose Morphometrie, biochemische bzw. Parameter der Endotheldysfunktion wren z. B um eine PV von 1. AGLA p. PDW auf eine p. PDW von 8. 0 zu heben Wahrsager wre bei einer n. PDW von 9. 5 eine Test Sensitivitt von 7. Spezifitt von 9. B A Y E S Calculator. Tabelle Kardio cerebrovaskulre Risikofaktoren Hypertonie focussierter Aspekt. Kumuliertes 1. 0 Jahres Risiko AR fr CVIAMI gemss baseline Data aus ELSA European Lacipidine Study on Atherosclerosis Motens Zanchetti et al, J Hypertension 1. Guidelines Hypertonie Management 1. WHOISH International Society of Hypertension.