History of invasive and interventional cardiology

The history of invasive and interventional cardiology is complex, with multiple groups working independently on similar technologies. Invasive and interventional cardiology is currently closely associated with cardiologists (physicians who treat the diseases of the heart), though the development and most of its early research and procedures were performed by diagnostic and interventional radiologists.

The birth of invasive cardiology

The history of invasive cardiology begins with the development of cardiac catheterization in 1711, when Stephen Hales placed catheters into the right and left ventricles of a living horse.[1] Variations on the technique were performed over the subsequent century, with formal study of cardiac physiology being performed by Claude Bernard in the 1840s.[2]

Catheterization of humans

The technique of angiography itself was first developed in 1927 by the Portuguese physician Egas Moniz at the University of Lisbon for cerebral angiography, the viewing of brain vasculature by X-ray radiation with the aid of a contrast medium introduced by catheter. Cardiac catheterization was first performed when Werner Forssmann, in 1929, created an incision in one of his left antecubital veins and inserted a catheter into his venous system. He then guided the catheter by fluoroscopy into his right atrium. Subsequently, he walked up a flight of stairs to the radiology department and documented the procedure by having a chest roentgenogram performed.[3] Over the next year, catheters were placed in a similar manner into the right ventricle, and measurements of pressure and cardiac output (using the Fick principle) were performed.[4]

In the early 1940s, André Cournand, in collaboration with Dickinson Richards, performed more systematic measurements of the hemodynamics of the heart.[5] For their work in the discovery of cardiac catheterization and hemodynamic measurements, Cournand, Forssmann, and Richards shared the Nobel Prize in Physiology or Medicine in 1956.

Development of the diagnostic coronary angiogram

In 1958, Interventional Radiologist, Dr. Charles Dotter began working on methods to visualize the coronary anatomy via sequential radiographic films. He invented a method known as occlusive aortography in an animal model. Occlusive aortography involved the transient occlusion of the aorta and subsequent injection of a small amount of radiographic contrast agent into the aortic root and subsequent serial x-rays to visualize the coronary arteries.[6] This method produced impressive images of the coronary anatomy. Dotter later reported that all the animals used in the procedure survived.

Later that same year, while performing an aortic root aortography, Mason Sones, a pediatric cardiologist at the Cleveland Clinic, noted that the catheter had accidentally entered the patient's right coronary artery. Before the catheter could be removed, 30cc of contrast agent had been injected.[7] While the patient went into ventricular fibrillation, the dangerous arrhythmia was terminated by Dr. Sones promptly performing a precordial thump which restored sinus rhythm. This became the world's first selective coronary arteriogram. Until that time, it was believed that even a small amount of contrast agent within a coronary artery would be fatal.

Until the 1950s, placing a catheter into either the arterial or venous system involved a "cut down" procedure, in which the soft tissues were dissected out of the way until the artery or vein was directly visualized and subsequently punctured by a catheter; this was known as the Sones technique. The percutaneous approach that is widely used today was developed by radiologist Sven-Ivar Seldinger in 1953.[8][9] This method was used initially for the visualization of the peripheral arteries. Percutaneous access of the artery or vein is still commonly known as the Seldinger technique. The use of the Seldinger technique for visualizing the coronary arteries was described by Ricketts and Abrams in 1962 and Judkins in 1967.[10][11]

By the late 1960s, Melvin Judkins had begun work on creating catheters that were specially shaped to reach the coronary arteries to perform selective coronary angiography. His initial work involved shaping stiff wires and comparing those shapes to radiographs of the ascending aorta to determine if the shape appeared promising. Then he would place the stiff wire inside a flexible catheter and use a heat-fixation method to permanently shape the catheter. In the first use of these catheters in humans, each catheter was specifically shaped to match the size and shape of the aorta of the subject. His work was documented in 1967, and by 1968 the Judkins catheters were manufactured in a limited number of fixed tip shapes.[12] Catheters in these shapes carry his name and are still used to this day for selective coronary angiography.

Dawn of the interventional era

The use of tapered Teflon dilating catheters for the treatment of atherosclerotic vascular disease was first described in 1964 by two interventional radiologists, Charles Dotter and Melvin Judkins, when they used it to treat a case of atherosclerotic disease in the superficial femoral artery of the left leg.[13][14] Building on their work and his own research involving balloon-tipped catheters, Andreas Gruentzig performed the first success percutaneous transluminal coronary angioplasty (known as PTCA or percutaneous coronary intervention (PCI)) on a human on September 16, 1977 at University Hospital, Zurich.[15] The results of the procedure were presented at the American Heart Association meeting two months later to a stunned audience of cardiologists. In the subsequent three years, Dr. Gruentzig performed coronary angioplasties in 169 patients in Zurich, while teaching the practice of coronary angioplasty to a field of budding interventional cardiologists. Ten years later, nearly 90 percent of these individuals were still alive.[15] By the mid-1980s, over 300,000 PTCAs were being performed on a yearly basis, equalling the number of bypass surgeries being performed for coronary artery disease.[16]

Soon after Andreas Gruentzig began performing percutaneous interventions on individuals with stable coronary artery disease, multiple groups described the use of catheter-delivered streptokinase for the treatment of acute myocardial infarction (heart attack).[17][18]

In the early years of coronary angioplasty, there were a number of serious complications. Abrupt vessel closure after balloon angioplasty occurred in approximately 1% of cases, often necessitating emergency bypass surgery. Vessel dissection was a frequent issue as a result of improper sizing of the balloon relative to the arterial diameter. Late restenosis occurred in as many as 30% of individuals who underwent PTCA, often causing recurrence of symptoms necessitating repeat procedures.

Development of the intracoronary stent

From the time of the initial percutaneous balloon angioplasty, it was theorized that devices could be placed inside the arteries as scaffolds to keep them open after a successful balloon angioplasty.[13] This did not become a reality in the cardiac realm until the first intracoronary stents were successfully deployed in coronary arteries in 1986.[19][20] The first stents used were self-expanding Wallstents. The use of intracoronary stents was quickly identified as a method to treat some complications due to PTCA,[19] and their use can decrease the incidence of emergency bypass surgery for acute complications post balloon angioplasty.[21]

It was quickly realized that restenosis rates were significantly lower in individuals who received an intracoronary stent when compared to those who underwent just balloon angioplasty.[22] A damper on the immediate use of intracoronary stents was subacute thrombosis. Subacute thrombosis rates with intracoronary stents proved to be about 3.7 percent, higher than the rates seen after balloon angioplasty.[20] Post-procedure bleeding was also an issue, due to the intense combination of anticoagulation and anti-platelet agents used to prevent stent thrombosis.

Stent technology improved rapidly, and in 1989 the Palmaz-Schatz balloon-expandable intracoronary stent was developed.[23][24] Initial results with the Palmaz-Schatz stents were excellent when compared to balloon angioplasty, with a significantly lower incidence of abrupt closure and peri-procedure heart attack.[25] Late restenosis rates with Palmaz-Schatz stents were also significantly improved when compared with balloon angioplasty.[26][27] However, mortality rates were unchanged compared to balloon angioplasty.[28] While the rates of subacute thrombosis and bleeding complications associated with stent placement were high, by 1999 nearly 85% of all PCI procedures included intracoronary stenting.[29]

In recognition of the focused training required by cardiologists to perform percutaneous coronary interventions and the rapid progression in the field of percutaneous coronary interventions, specialized fellowship training in the field of Interventional Cardiology was instituted in 1999.[16]

Changes in post-procedure medications

Through the 1990s and beyond, various incremental improvements were made in balloon and stent technology, as well as newer devices, some of which are still in use today while many more have fallen into disuse. As important as balloon and stent technology had been, it was becoming obvious that the anticoagulation and anti-platelet regimen that individuals received post-intervention was at least as important. Trials in the late 1990s revealed that anticoagulation with warfarin was not required post balloon angioplasty or stent implantation, while intense anti-platelet regimens and changes in procedural technique (most importantly, making sure that the stent was well opposed to the walls of the coronary artery) improved short term and long term outcomes.[30] Many different antiplatelet regimens were evaluated in the 1990s and the turn of the 21st century, with the optimal regimen in an individual patient still being up for debate.

The drug eluting stent era

With the high use of intracoronary stents during PCI procedures, the focus of treatment changed from procedural success to prevention of recurrence of disease in the treated area (in-stent restenosis). By the late 1990s it was generally acknowledged among cardiologists that the incidence of in-stent restenosis was between 15 and 30%, and possibly higher in certain subgroups of individuals.[29] Stent manufacturers experimented with (and continue to experiment with) a number of chemical agents to prevent the neointimal hyperplasia that is the cause of in-stent restenosis.

One of the first products of the new focus on preventing late events (such as in stent restenosis and late thrombosis) was the heparin-coated Palmaz-Schatz stent.[31] These coated stents were found to have a lower incidence of subacute thrombosis than bare metal stents.[32]

At approximately the same time, Cordis (a division of Johnson & Johnson) was developing the Cypher stent, a stent that would release sirolimus (a chemotherapeutic agent) over time. The first study of these individuals revealed an incredible lack of restenosis (zero percent restenosis) at six months.[33] This led to the approval for the stent to be used in Europe in April 2002.[34] Further trials with the Cypher stent revealed that restenosis did occur in some individuals with high risk features (such as long areas of stenosis or a history of diabetes mellitus), but that the restenosis rate was significantly lower than with bare metal stents (3.2 percent compared to 35.4 percent).[35] About a year after approval in Europe, the United States FDA approved the use of the Cypher stent as the first drug-eluting stent for use in the general population in the United States.[36]

With the significantly lower restenosis rates of drug eluting stents compared to bare metal stents, the interventional cardiology community began using these stents as soon as they became available. Cordis, the manufacturer of the Cypher drug eluting stent, was not able to keep up with the demand for these stents when they first entered the market. This fueled a rationing of Cypher stents; they were used on difficult anatomy and high risk individuals. At the time there was a fear by the general population that these drug eluting stents would not be used on individuals who could not afford them (as they cost significantly more than the bare metal stents of the era).

Concurrent with the development of the Cypher stent, Boston Scientific started development of the Taxus stent. The Taxus stent was the Express2 metal stent, which was in general use for a number of years,[37] with a copolymer coating of paclitaxel that inhibited cell replication. As with the Cypher stent before it, the first trials of the Taxus stent revealed no evidence of in-stent restenosis at six months after the procedure,[38] while later studies showed some restenosis, at a rate much lower than the bare metal counterpart.[39] Based on these trials, the Taxus stent was approved for use in Europe in 2003. With further study,[40] the FDA approved the use of the Taxus stent in the United States in March 2004.[41]

By the end of 2004, drug-eluting stents were used in nearly 80 percent of all percutaneous coronary interventions.[42]

Trials of heparin-coated stents could not match the significant decrease in restenosis rates seen with the Cypher and Taxus stents. With the increased supply in the chemotherapeutic drug-eluting stents available, the use of heparin-coated stents waned.

Modern controversies in interventional cardiology

The field of interventional cardiology has had a number of controversies since its inception. In part this is because of the dawning of the randomized control trial as the marker of a successful procedure. This is worsened by the rapid changes in the field of interventional cardiology. Procedures would be used soon after they are described in the literature or at conferences, with trial data determining if the procedure improves outcomes lagging behind by years due to the strict protocols and long follow-up of patients necessary to test the procedure. By the time the trials were published, they would be considered out of date, as they did not reflect the current practice in the field. This led to the inception and use of a number of procedures and devices in the interventional realm that have fallen out of practice due to their being found to not improve outcomes after formal trials have been performed.

Roles of bypass surgery and intracoronary stents for coronary artery disease

Another source of controversy in the field of interventional cardiology is the overlapping roles of PCI and coronary artery bypass surgery for individuals with coronary artery disease. This area has been studied in a number of trials since the early 1990s.[43][44][45] Unfortunately, due to the rapid changes in technique in both bypass surgery as well as PCI, added to the better understanding of the role of intense pharmacologic therapy in individuals with coronary artery disease, questions still remain on the best form of therapy in many subgroups of patients. Multiple ongoing studies hope to tease out which individuals do better with PCI and which do better with CABG,[46] but in general each case is individualized to the patient and the relative comfort level of the interventional cardiologist and the cardiothoracic surgeon.

The role of PCI in individuals without symptoms of ischemic heart disease

In the vast majority of cases, percutaneous coronary interventions do not improve mortality when compared to optimal medical therapy in the stable individual. This is, of course, not true in the unstable individual, such as in the setting after a myocardial infarction (heart attack). Even in the stable individuals, however, there are a number of subsets in which there is a mortality benefit that is attributed to PCI.

Subsequently, at the 2007 meeting of the American College of Cardiology (ACC), data from the COURAGE trial was presented, suggested that the combination of PCI and intensive (optimal) medical therapy did not reduce the incidence of death, heart attacks, or stroke compared to intensive medical therapy alone.[47] Critics of the trial state that the trial did not take into account the improvement in symptoms attributed to PCI. Also, the data that was presented was an intention to treat analysis, and that there was a (possibly) significant crossover from the medical therapy arm to the PCI arm of the study. It should also be noted that the optimal medical therapy seen in the COURAGE trial is significantly more aggressive than the current guidelines of the ACC and are not commonly seen in the general cardiology clinic. As with any large clinical trial, the therapies available had changed from when the trial was designed to when the results were presented. In particular, drug eluting stents, while commonly used in practice at the time the results of the trial were presented, were used in less than 5 percent of individuals in the trial.

The safety of drug-eluting stents

When the results of the first trials of drug-eluting stents were published, there was a general feeling in the interventional cardiology community that these devices would be part of the perfect revascularization regimen for coronary artery disease. With the very low restenosis rates of the RAVEL[33] and SIRIUS[35] trials, interventions were performed on more complex blockages in the coronary arteries, under the assumption that the results in real life would mimic the results in the trials. The antiplatelet regimens that were advised for the drug eluting stents were based on the early trials of these stents. Based on these trials, the antiplatelet regimen was a combination of aspirin and clopidogrel for 3 months when Cypher stents were used,[35] and 9 months when Taxus stents were used,[48] followed by aspirin indefinitely.

Soon, case reports started being published regarding late stent thrombosis.[49] At the 2006 annual meeting of the American College of Cardiology, preliminary results of the BASKET-LATE trial were presented, which showed a slight increase in late thrombosis associated with drug eluting stents over bare metal stents.[50] However, this increase was not statistically significant, and further data would have to be collected. Further data published over the following year had conflicting results,[51] and it was unclear whether stent thrombosis was truly higher when compared to bare metal stents. During this time of uncertainty, many cardiologists started extending the dual antiplatelet regimen of aspirin and clopidogrel in these individuals, as some data suggested that it may prevent late thrombosis.[52]

The FDA held an expert panel in December 2006 to go over the data presented by Cordis and Boston Scientific to determine if drug eluting stents should be considered less safe than bare metal stents.[53] It became evident at the meeting that with all the data published there were varied definitions of late thrombosis and key differences in the types of lesions in different studies, hampering analysis of the data.[42] It was also noted that with the advent of drug eluting stents, interventional cardiologists began performing procedures on more complex lesions, subsequently using the drug eluting stents in "off label" coronary artery lesions, which would otherwise go untreated or for bypass surgery.[42] The FDA advisory board reiterated the ACC guidelines that clopidogrel should be continued for 12 months after drug eluting stent placement in individuals who are at low risk for bleeding.[54][55]

See also

References

  1. ↑ Mueller RL, Sanborn TA (1995). "The history of interventional cardiology: cardiac catheterization, angioplasty, and related interventions". Am Heart J. 129 (1): 146–72. doi:10.1016/0002-8703(95)90055-1. PMID 7817908.
  2. ↑ Cournand A (1975). "Cardiac catheterization; development of the technique, its contributions to experimental medicine, and its initial applications in man". Acta Med Scand Suppl. 579: 3–32. PMID 1101653.
  3. ↑ Forssmann W (1929). "Sondierung des rechten Herzens". Klin Wochenschr. 8 (45): 2085–2087. doi:10.1007/BF01875120.
  4. ↑ Klein O. (1930). "Zur Bestimmung des zerkulatorischen minutens Volumen nach dem Fickschen Prinzip". Munich Med Wochenschr (77): 1311.
  5. ↑ Cournand A, Riley RL, Breed ES, Baldwin ED, Richards DW, Lester MS, Jones M (1945). "Measurement of Cardiac Output in Man Using the Technique of Catheterization of the Right Auricle or Ventricle". J Clin Invest. 24 (1): 106–16. doi:10.1172/JCI101570. PMC 435435. PMID 16695180.
  6. ↑ Dotter CT, Frische LH (1958). "Visualization of the coronary circulation by occlusion aortography: a practical method". Radiology. 71 (4): 502–24. doi:10.1148/71.4.502. PMID 13591535.
  7. ↑ Connolly JE (2002). "The Development of Coronary Artery Surgery: Personal Recollections". Tex Heart Inst J. 29 (1): 10–4. PMC 101261. PMID 11995842.
  8. ↑ Seldinger SI. (1953). "Catheter replacement of the needle in percutaneous arteriography; a new technique". Acta Radiol. 39 (5): 368–76. doi:10.3109/00016925309136722. PMID 13057644.
  9. ↑ Higgs ZC, Macafee DA, Braithwaite BD, Maxwell-Armstrong CA (2005). "The Seldinger technique: 50 years on". Lancet. 366 (9494): 1407–9. doi:10.1016/S0140-6736(05)66878-X. PMID 16226619.
  10. ↑ Ricketts HJ, Abrams HL (1962). "Percutaneous selective coronary cine arteriography". JAMA. 181 (7): 620–4. doi:10.1001/jama.1962.03050330050011. PMID 14492075.
  11. ↑ Judkins MP. (1967). "Selective coronary arteriography. A percutaneous transfemoral technique". Radiology. 89 (5): 815–24. doi:10.1148/89.5.815. PMID 6048074.
  12. ↑ "Tribute to a Legend in Invasive/Interventional Cardiology: Melvin P. Judkins, M.D. (1922–85)". Society For Cardiovascular Angiography And Interventions. Archived from the original on 2007-02-07. Retrieved 2007-04-08.
  13. 1 2 Dotter CT, Judkins MP (1964). "Transluminal treatment of arteriosclerotic obstruction. Description of a new technique and a preliminary report of its application". Circulation. 30 (5): 654–70. doi:10.1161/01.CIR.30.5.654. PMID 14226164.
  14. ↑ Payne MM. (2 April 2001). "Charles Theodore Dotter: The Father of Intervention". Tex Heart Inst J. 28 (1): 28–38. PMC 101126. PMID 11330737.
  15. 1 2 King SB 3rd, Schlumpf M. (1993). "Ten-year completed follow-up of percutaneous transluminal coronary angioplasty: the early Zurich experience". J Am Coll Cardiol. 22 (2): 353–60. doi:10.1016/0735-1097(93)90037-2. PMID 8335804.
  16. 1 2 Donald S. Baim; William Grossman (2000). Grossman's Cardiac Catheterization, Angiography, and Intervention. Philadelphia, PA: Lippincott Williams & Wilkins. p. ix. ISBN 978-0-683-30741-2.
  17. ↑ Rentrop KP, Blanke H, Karsch KR, Wiegand V, Kostering H, Oster H, Leitz K (1979). "Acute myocardial infarction: intracoronary application of nitroglycerin and streptokinase". Clin Cardiol. 2 (5): 354–63. doi:10.1002/clc.4960020507. PMID 121799.
  18. ↑ Ganz W, Buchbinder N, Marcus H, Mondkar A, Maddahi J, Charuzi Y, O'Connor L, Shell W, Fishbein MC, Kass R, Miyamoto A, Swan HJ (1981). "Intracoronary thrombolysis in evolving myocardial infarction". Am Heart J. 101 (1): 4–13. doi:10.1016/0002-8703(81)90376-8. PMID 6450527.
  19. 1 2 Sigwart U, Puel J, Mirkovitch V, Joffre F, Kappenberger L (1987). "Intravascular stents to prevent occlusion and restenosis after transluminal angioplasty". N Engl J Med. 316 (12): 701–6. doi:10.1056/NEJM198703193161201. PMID 2950322.
  20. 1 2 Serruys PW, Kutryk MJ, Ong AT (2006). "Coronary-artery stents". N Engl J Med. 354 (5): 483–95. doi:10.1056/NEJMra051091. PMID 16452560.
  21. ↑ Roubin GS, Cannon AD, Agrawal SK, Macander PJ, Dean LS, Baxley WA, Breland J (1992). "Intracoronary stenting for acute and threatened closure complicating percutaneous transluminal coronary angioplasty". Circulation. 85 (3): 916–27. doi:10.1161/01.cir.85.3.916. PMID 1537128.
  22. ↑ Serruys PW; Strauss BH; Beatt KJ; Bertrand ME; Puel J; Rickards AF; Meier B; Goy JJ; Vogt P (1991). "Angiographic follow-up after placement of a self-expanding coronary-artery stent". N Engl J Med. 324 (1): 13–7. doi:10.1056/NEJM199101033240103. hdl:1765/4410. PMID 1984159.
  23. ↑ Palmaz JC, Sibbitt RR, Reuter SR, Tio FO, Rice WJ (1985). "Expandable intraluminal graft: a preliminary study. Work in progress". Radiology. 156 (1): 73–7. doi:10.1148/radiology.156.1.3159043. PMID 3159043.
  24. ↑ Palmaz JC, Windeler SA, Garcia F, Tio FO, Sibbitt RR, Reuter SR (1986). "Atherosclerotic rabbit aortas: expandable intraluminal grafting". Radiology. 160 (3): 723–6. doi:10.1148/radiology.160.3.2942964. PMID 2942964.
  25. ↑ Schatz RA; Baim DS; Leon M; Ellis SG; Goldberg S; Hirshfeld JW; Cleman MW; Cabin HS; Walker C (1991). "Clinical experience with the Palmaz-Schatz coronary stent. Initial results of a multicenter study". Circulation. 83 (1): 148–61. doi:10.1161/01.cir.83.1.148. PMID 1984878.
  26. ↑ Serruys PW; de Jaegere P; Kiemeneij F; Macaya C; Rutsch W; Heyndrickx G; Emanuelsson H; Marco J; Legrand V (1994). "A comparison of balloon-expandable-stent implantation with balloon angioplasty in patients with coronary artery disease". N Engl J Med. 331 (8): 489–95. doi:10.1056/NEJM199408253310801. hdl:1765/58398. PMID 8041413.
  27. ↑ Fischman DL; Leon MB; Baim DS; Schatz RA; Savage MP; Penn I; Detre K; Veltri L; Ricci D (1994). "A randomized comparison of coronary-stent placement and balloon angioplasty in the treatment of coronary artery disease". N Engl J Med. 331 (8): 496–501. doi:10.1056/NEJM199408253310802. PMID 8041414.
  28. ↑ Brophy JM, Belisle P, Joseph L (2003). "Evidence for use of coronary stents. A hierarchical bayesian meta-analysis". Annals of Internal Medicine. 138 (10): 777–86. CiteSeerX 10.1.1.510.2007. doi:10.7326/0003-4819-138-10-200305200-00005. PMID 12755549.
  29. 1 2 Holmes DR Jr, Savage M, LaBlanche JM, Grip L, Serruys PW, Fitzgerald P, Fischman D, Goldberg S, Brinker JA, Zeiher AM, Shapiro LM, Willerson J, Davis BR, Ferguson JJ, Popma J, King SB 3rd, Lincoff AM, Tcheng JE, Chan R, Granett JR, Poland M (2002). "Results of Prevention of REStenosis with Tranilast and its Outcomes (PRESTO) trial". Circulation. 106 (10): 1243–50. doi:10.1161/01.CIR.0000028335.31300.DA. PMID 12208800.
  30. ↑ Colombo A, Hall P, Nakamura S, Almagor Y, Maiello L, Martini G, Gaglione A, Goldberg SL, Tobis JM (1995). "Intracoronary stenting without anticoagulation accomplished with intravascular ultrasound guidance". Circulation. 91 (6): 1676–88. doi:10.1161/01.cir.91.6.1676. PMID 7882474.
  31. ↑ Serruys PW, van Hout B, Bonnier H, Legrand V, Garcia E, Macaya C, Sousa E, van der Giessen W, Colombo A, Seabra-Gomes R, Kiemeneij F, Ruygrok P, Ormiston J, Emanuelsson H, Fajadet J, Haude M, Klugmann S, Morel MA (1998). "Randomised comparison of implantation of heparin-coated stents with balloon angioplasty in selected patients with coronary artery disease (Benestent II)". Lancet. 352 (9129): 673–81. doi:10.1016/S0140-6736(97)11128-X. PMID 9728982.
  32. ↑ Gupta V, Aravamuthan BR, Baskerville S, Smith SK, Gupta V, Lauer MA, Fischell TA (2004). "Reduction of subacute stent thrombosis (SAT) using heparin-coated stents in a large-scale, real world registry". J Invasive Cardiol. 16 (6): 304–10. PMID 15155999.
  33. 1 2 Morice MC, Serruys PW, Sousa JE, Fajadet J, Ban Hayashi E, Perin M, Colombo A, Schuler G, Barragan P, Guagliumi G, Molnar F, Falotico R, RAVEL Study Group. Randomized Study with the Sirolimus-Coated Bx Velocity Balloon-Expandable Stent in the Treatment of Patients with de Novo Native Coronary Artery Lesions. (2002). "A randomized comparison of a sirolimus-eluting stent with a standard stent for coronary revascularization". N Engl J Med. 346 (23): 1773–80. doi:10.1056/NEJMoa012843. hdl:1765/8459. PMID 12050336.
  34. ↑ "Cordis' CYPHER TM Sirolimus-eluting Stent Receives CE Mark Approval" (PDF). Cordis Corporation. April 15, 2002. Archived from the original (PDF) on October 17, 2006. Retrieved 2007-04-09.
  35. 1 2 3 Moses JW, Leon MB, Popma JJ, Fitzgerald PJ, Holmes DR, O'Shaughnessy C, Caputo RP, Kereiakes DJ, Williams DO, Teirstein PS, Jaeger JL, Kuntz RE, SIRIUS Investigators (2003). "Sirolimus-eluting stents versus standard stents in patients with stenosis in a native coronary artery". N Engl J Med. 349 (14): 1315–23. doi:10.1056/NEJMoa035071. PMID 14523139.
  36. ↑ "FDA Approves Drug-Eluting Stent for Clogged Heart Arteries". U.S. Food And Drug Administration. April 24, 2003. Archived from the original on April 3, 2007. Retrieved 2007-04-08.
  37. ↑ "Express and Express2 Monorail and Over-the-Wire Coronary Stent Systems" (PDF). United States Food And Drug Administration. September 11, 2002. Retrieved 2007-04-11.
  38. ↑ Grube E, Silber S, Hauptmann KE, Mueller R, Buellesfeld L, Gerckens U, Russell ME (2003). "TAXUS I: six- and twelve-month results from a randomized, double-blind trial on a slow-release paclitaxel-eluting stent for de novo coronary lesions". Circulation. 107 (1): 38–42. doi:10.1161/01.CIR.0000047700.58683.A1. PMID 12515740.
  39. ↑ Colombo A, Drzewiecki J, Banning A, Grube E, Hauptmann K, Silber S, Dudek D, Fort S, Schiele F, Zmudka K, Guagliumi G, Russell ME, TAXUS II Study Group (2003). "Randomized study to assess the effectiveness of slow- and moderate-release polymer-based paclitaxel-eluting stents for coronary artery lesions". Circulation. 108 (7): 788–94. doi:10.1161/01.CIR.0000086926.62288.A6. PMID 12900339.
  40. ↑ Stone GW, Ellis SG, Cox DA, Hermiller J, O'Shaughnessy C, Mann JT, Turco M, Caputo R, Bergin P, Greenberg J, Popma JJ, Russell ME, TAXUS-IV Investigators (2004). "A polymer-based, paclitaxel-eluting stent in patients with coronary artery disease". N Engl J Med. 350 (3): 221–31. doi:10.1056/NEJMoa032441. PMID 14724301.
  41. ↑ "New Device Approval: TAXUS Express2 Paclitaxel-Eluting Coronary Stent System". U. S. Food And Drug Administration. March 4, 2004. Archived from the original on October 10, 2006. Retrieved 2007-04-08.
  42. 1 2 3 Maisel WH. (2007). "Unanswered questions—drug-eluting stents and the risk of late thrombosis". N Engl J Med. 356 (10): 981–4. doi:10.1056/NEJMp068305. PMID 17296826.
  43. ↑ RITA Investigators (1993). "Coronary angioplasty versus coronary artery bypass surgery: the Randomized Intervention Treatment of Angina (RITA) trial". Lancet. 341 (8845): 573–80. doi:10.1016/0140-6736(93)90348-K. PMID 8094826.
  44. ↑ The Bypass Angioplasty Revascularization Investigation (BARI) Investigators. (1996). "Comparison of coronary bypass surgery with angioplasty in patients with multivessel disease". N Engl J Med. 335 (4): 217–25. doi:10.1056/NEJM199607253350401. PMID 8657237.
  45. ↑ Rodriguez A, Bernardi V, Navia J, Baldi J, Grinfeld L, Martinez J, Vogel D, Grinfeld R, Delacasa A, Garrido M, Oliveri R, Mele E, Palacios I, O'Neill W (2001). "Argentine Randomized Study: Coronary Angioplasty with Stenting versus Coronary Bypass Surgery in patients with Multiple-Vessel Disease (ERACI II): 30-day and one-year follow-up results. ERACI II Investigators". J Am Coll Cardiol. 37 (1): 51–8. doi:10.1016/S0735-1097(00)01052-4. PMID 11153772.
  46. ↑ "SYNTAX Study: TAXUS Drug-Eluting Stent Versus Coronary Artery Bypass Surgery for the Treatment of Narrowed Arteries". U.S. National Institute of Health. Retrieved 2007-04-08.
  47. ↑ Hochman JS, Steg PG (2007). "Does Preventive PCI Work?". N Engl J Med. 356 (15): 1572–4. doi:10.1056/NEJMe078036. PMID 17387128.
  48. ↑ Mehta SR, Yusuf S, Peters RJ, Bertrand ME, Lewis BS, Natarajan MK, Malmberg K, Rupprecht H, Zhao F, Chrolavicius S, Copland I, Fox KA, Clopidogrel in Unstable angina to prevent Recurrent Events trial (CURE) Investigators (2001). "Effects of pretreatment with clopidogrel and aspirin followed by long-term therapy in patients undergoing percutaneous coronary intervention: the PCI-CURE study". Lancet. 358 (9281): 527–33. doi:10.1016/S0140-6736(01)05701-4. PMID 11520521.
  49. ↑ Camenzind E, Steg PG, Wijns W (2007). "Stent thrombosis late after implantation of first-generation drug-eluting stents: a cause for concern". Circulation. 115 (11): 1440–55. doi:10.1161/CIRCULATIONAHA.106.666800. PMID 17344324.
  50. ↑ Wood, Shelley (March 14, 2006). "BASKET-LATE: High cardiac death and MI rates in DES-treated patients fuel late stent thrombosis debate". TheHeart.org. Retrieved 2007-04-15.
  51. ↑ Spaulding C, Daemen J, Boersma E, Cutlip DE, Serruys PW (2007). "A pooled analysis of data comparing sirolimus-eluting stents with bare-metal stents". N Engl J Med. 356 (10): 989–97. CiteSeerX 10.1.1.424.7486. doi:10.1056/NEJMoa066633. PMID 17296825.
  52. ↑ Eisenstein EL, Anstrom KJ, Kong DF, Shaw LK, Tuttle RH, Mark DB, Kramer JM, Harrington RA, Matchar DB, Kandzari DE, Peterson ED, Schulman KA, Califf RM (2007). "Clopidogrel use and long-term clinical outcomes after drug-eluting stent implantation". JAMA. 297 (2): 159–68. doi:10.1001/jama.297.2.joc60179. PMID 17148711.
  53. ↑ "Circulatory System Devices Panel Advisory Meetings". United States Food And Drug Administration. December 8, 2006. Retrieved 2007-04-15.
  54. ↑ Gross, Neal (December 8, 2006). "Circulatory System Devices Advisory Panel" (RTF). United States Food And Drug Administration. Retrieved 2007-04-16.
  55. ↑ Smith SC Jr, Feldman TE, Hirshfeld JW Jr, Jacobs AK, Kern MJ, King SB 3rd, Morrison DA, O'Neil WW, Schaff HV, Whitlow PL, Williams DO, Antman EM, Adams CD, Anderson JL, Faxon DP, Fuster V, Halperin JL, Hiratzka LF, Hunt SA, Nishimura R, Ornato JP, Page RL, Riegel B, American College of Cardiology/American Heart Association Task Force on Practice Guidelines; ACC/AHA/SCAI Writing Committee to Update 2001 Guidelines for Percutaneous Coronary Intervention (2006). "ACC/AHA/SCAI 2005 guideline update for percutaneous coronary intervention: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/SCAI Writing Committee to Update 2001 Guidelines for Percutaneous Coronary Intervention)". Circulation. 113 (7): e166–286. doi:10.1161/CIRCULATIONAHA.106.173220. PMID 16490830.
This article is issued from Offline. The text is licensed under Creative Commons - Attribution - Sharealike. Additional terms may apply for the media files.