Global Supplier Strategy for Market Penetration & Partnership Options (Niche Suppliers vs. National Leaders) in the Massachusetts Cardiology & Vascular Surgery Tools and Devices Market for Cardiac Operating Rooms and Angioplasty Suites
Curator: Aviva Lev-Ari, PhD, RN
The ecosystem of Cardiac and Vascular Surgery for Repair or Replacement by Implantation of a new blood vessel or medical device covers the following procedure-related devices and tools now in use:
- Arterial catheterization kit
- Embolectomy catheters
- Occlusion catheter
- Coronary stents
- Neurovascular stents
- Carotid stents
- External and internal carotid shunts
- Peripheral stents
- Biliary stents
- Micro vascular clips
- Stainless steel tunneler vascular graft
- Cardiopulmonary bypass vascular catheter
- Coronary stent graft system
- Catheter tip occluder
- Synthetic/biological composite vascular graft
- Valvulotome tools
- Aortic Valve
- Mitral Valve
- Angioplasty Guided Wires
No Aorta valve suppliers in MA. The National Leader supplier Edwards Lifesciences and its SAPIEN product for Transcatheter Aortic-Valve Implantation (TAVI) and Replacement (TAVR) is covered in Executive Compensation and Comparator Group Definition in the Cardiac and Vascular Medical Devices Sector: A Bright Future for Edwards Lifesciences Corporation in the Transcatheter Heart Valve Replacement Market 6/20/2012
Medical Devices Market in Massachusetts: Product Concentration Ratios (1 to 10) by Product and Partnership Target Advantage – Niche Suppliers vs. National Leader in the Cardiology & Vascular Surgery Tools and Devices in use in Cardiac Operating Rooms and in Angioplasty Suites
|
Industry Concentration Ratios per Product Line in the Cardiac and Vascular Medical Devices Segments |
|||||||||
|
A |
B |
C |
D |
E |
F |
G |
H |
I |
J |
|
US comparison |
MA comparison |
||||||||
| Cardiology & Vascular Surgery Tools and Devices in use |
Global Suppliers |
US Suppliers |
Market share |
Global ratio |
Index |
MA Suppliers |
Market share |
Global ratio |
Index |
| Arterial catheterization kit |
4 |
6 |
0.09 |
0.40 |
5.6 |
2 |
0.14 |
0.67 |
3.6 |
| Embolectomy catheters |
11 |
28 |
0.03 |
0.28 |
1.9 |
3 |
0.07 |
0.79 |
2.4 |
| Occlusion catheter |
1 |
7 |
0.11 |
0.13 |
2.8 |
3 |
0.20 |
0.25 |
2.4 |
| Coronary stents |
11 |
34 |
0.02 |
0.24 |
1.7 |
2 |
0.07 |
0.85 |
2.6 |
| Neurovascular stents |
2 |
6 |
0.11 |
0.25 |
4.5 |
1 |
0.25 |
0.67 |
5.5 |
| Carotid stents |
1 |
12 |
0.07 |
0.08 |
1.7 |
1 |
0.33 |
0.50 |
5.5 |
| External and internal carotid shunts |
2 |
5 |
0.13 |
0.29 |
5.5 |
2 |
0.20 |
0.50 |
3.7 |
| Peripheral stents |
0 |
7 |
0.13 |
0.00 |
1.0 |
1 |
0.50 |
0.00 |
1.0 |
| Biliary stents |
7 |
13 |
0.05 |
0.35 |
3.1 |
1 |
0.11 |
0.88 |
3.6 |
| Micro vascular clips |
3 |
6 |
0.10 |
0.33 |
5.2 |
2 |
0.17 |
0.60 |
3.7 |
| Stainless steel tunneler vascular graft |
3 |
3 |
0.14 |
0.50 |
10.0 |
1 |
0.20 |
0.75 |
5.1 |
| Cardiopulmonary bypass vascular catheter |
14 |
39 |
0.02 |
0.26 |
1.6 |
5 |
0.05 |
0.74 |
2.0 |
| Coronary stent graft system |
0 |
6 |
0.14 |
0.00 |
1.0 |
1 |
0.50 |
0.00 |
1.0 |
| Catheter tip occluder |
1 |
6 |
0.13 |
0.14 |
3.3 |
2 |
0.25 |
0.33 |
3.3 |
| Synthetic/biological composite vascular graft |
3 |
5 |
0.11 |
0.38 |
6.3 |
2 |
0.17 |
0.60 |
3.7 |
| Valvulotome tools |
3 |
6 |
0.10 |
0.33 |
5.2 |
1 |
0.20 |
0.75 |
5.1 |
| Aortic Valve |
2 |
9 |
0.08 |
0.18 |
2.9 |
0 |
0.33 |
1.00 |
10.0 |
| Mitral Valve |
4 |
7 |
0.08 |
0.36 |
4.8 |
0 |
0.20 |
1.00 |
6.4 |
| Angioplasty Guided Wires |
8 |
11 |
0.05 |
0.42 |
3.7 |
2 |
0.09 |
0.80 |
3.0 |
|
126 |
27 |
||||||||
| Source for A, B, C, G – http://www.medicregister.com | |||||||||
| Source for D,E,F,H,I,J – Computed ratios per formulas below byAviva Lev-Ari, PhD, RN | |||||||||
| D = 1/(1+B+C) = projected market share assuming non-differential production capacity | |||||||||
| E = B/(B+C) = fraction of global among all suppliers | |||||||||
| F = D*E*$F$24+1 = product of “D” and “E”, scaled to be in the range from 1 to 10 | |||||||||
| “H” is the same as “D” but with MA suppliers replacing “US suppliers” | |||||||||
| “I” is the same as “E” but with MA suppliers replacing “US suppliers” | |||||||||
| “J” is the same as “F” but with MA suppliers replacing “US suppliers” | |||||||||
Product Advantage for Partnership with Niche Suppliers in MA
|
Product Concentration Ratio (PRC) for Tools and Devices in use in Cardiology & Vascular Surgery |
Targeting a Niche Supplier based in Massachusetts |
Aiming at the Industry Leader |
| Arterial catheterization kitPRC = 3.6 | Lemaitre Vascular, Inc. www.lemaitre.comBurlington
Weston |
|
| External and internal carotid shuntsPRC = 3.7 | Bard Electrophysiology www.bardep.comLowell
Lemaitre Vascular, Inc. www.lemaitre.com Burlington |
|
| Micro vascular clipsPRC = 3.7 | Lemaitre Vascular, Inc. www.lemaitre.comBurlington
Life Instrument Corporation www.lifeinstruments.com Braintree |
|
| Stainless steel tunneler vascular graftPRC = 5.1 | Lemaitre Vascular, Inc. www.lemaitre.comBurlington | |
| Cardiopulmonary bypass vascular catheterPRC = 2 | Abiomed, Inc. www.abiomed.comDanvers
Vortex Medical Inc www.angiovac.com Norwell Lemaitre Vascular, Inc. www.lemaitre.com Burlington Clinical Instruments Intl., Inc. Southbridge Weston |
|
| Coronary stent graft systemPRC = 2.6 | Lemaitre Vascular, Inc. www.lemaitre.comBurlington | |
| Catheter tip occluderPRC = 2.4 | Lemaitre Vascular, Inc. www.lemaitre.comBurlington
Clinical Instruments Intl., Inc. Southbridge |
|
| Valvulotome toolsPRC = 5.1 | Lemaitre Vascular, Inc. www.lemaitre.comBurlington |
Product Advantage for Partnership with National Leader in MA
| Cardiology & Vascular Surgery Tools and Devices in use | Niche Supplier based in Massachusetts | Industry Leader |
| Neurovascular stentsPRC = 5.5 | Boston Scientific Corporation www.bostonscientific.comNatick | |
| Carotid stents PRC = 5.5 | Boston Scientific Corporation www.bostonscientific.comNatick | |
| Peripheral stentsPRC = 1 | Boston Scientific Corporation www.bostonscientific.comNatick | |
| Biliary stentsPRC = 3.6 | Boston Scientific Corporation www.bostonscientific.comNatick |
Product Advantage for Partnership with Niche Suppliers and National Leader in MA
| Cardiology & Vascular Surgery Tools and Devices in use | Niche Supplier based in Massachusetts | Industry Leader |
| Embolectomy cathetersPRC = 2.4 | Lemaitre Vascular, Inc. www.lemaitre.comBurlington
Clinical Instruments Intl., Inc. Southbridge |
Boston Scientific Corporation www.bostonscientific.comNatick |
| Occlusion catheterPRC = 2.4 | Lemaitre Vascular, Inc. www.lemaitre.comBurlington
Telemed Systems Inc. www.telemedsystems.com Hudson |
Boston Scientific Corporation www.bostonscientific.comNatick |
| Coronary stentsPRC = 2.6 | Lemaitre Vascular, Inc. www.lemaitre.comBurlington | Boston Scientific Corporation www.bostonscientific.comNatick |
| Synthetic/biological composite vascular graftPRC = 3.7 | Lemaitre Vascular, Inc. www.lemaitre.comBurlington | Boston Scientific Corporation www.bostonscientific.comNatick |
| Angioplasty Guided WiresPRC = 3.0 | Arrow International, Walrus DivisionWoburn | Boston Scientific Corporation www.bostonscientific.comNatick |
Source:
http://www.medicregister.com/Cardiology_Vascular_Surgery/Categories/cid2.htm
Penetration Strategy for a Global Supplier Targeting the US Market in Massachusetts
Customized predictions of penetration cost and estimation of potential revenues based on the industry segment concentration ratios in the Table above per Partnership Option are part of an Actionable Strategic Market Entry Plan in Massachusetts.
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PUT IT IN CONTEXT OF CANCER CELL MOVEMENT
The contraction of skeletal muscle is triggered by nerve impulses, which stimulate the release of Ca2+ from the sarcoplasmic reticuluma specialized network of internal membranes, similar to the endoplasmic reticulum, that stores high concentrations of Ca2+ ions. The release of Ca2+ from the sarcoplasmic reticulum increases the concentration of Ca2+ in the cytosol from approximately 10-7 to 10-5 M. The increased Ca2+ concentration signals muscle contraction via the action of two accessory proteins bound to the actin filaments: tropomyosin and troponin (Figure 11.25). Tropomyosin is a fibrous protein that binds lengthwise along the groove of actin filaments. In striated muscle, each tropomyosin molecule is bound to troponin, which is a complex of three polypeptides: troponin C (Ca2+-binding), troponin I (inhibitory), and troponin T (tropomyosin-binding). When the concentration of Ca2+ is low, the complex of the troponins with tropomyosin blocks the interaction of actin and myosin, so the muscle does not contract. At high concentrations, Ca2+ binding to troponin C shifts the position of the complex, relieving this inhibition and allowing contraction to proceed.
Figure 11.25
Association of tropomyosin and troponins with actin filaments. (A) Tropomyosin binds lengthwise along actin filaments and, in striated muscle, is associated with a complex of three troponins: troponin I (TnI), troponin C (TnC), and troponin T (TnT). In (more ) Contractile Assemblies of Actin and Myosin in Nonmuscle Cells
Contractile assemblies of actin and myosin, resembling small-scale versions of muscle fibers, are present also in nonmuscle cells. As in muscle, the actin filaments in these contractile assemblies are interdigitated with bipolar filaments of myosin II, consisting of 15 to 20 myosin II molecules, which produce contraction by sliding the actin filaments relative to one another (Figure 11.26). The actin filaments in contractile bundles in nonmuscle cells are also associated with tropomyosin, which facilitates their interaction with myosin II, probably by competing with filamin for binding sites on actin.
Figure 11.26
Contractile assemblies in nonmuscle cells. Bipolar filaments of myosin II produce contraction by sliding actin filaments in opposite directions. Two examples of contractile assemblies in nonmuscle cells, stress fibers and adhesion belts, were discussed earlier with respect to attachment of the actin cytoskeleton to regions of cell-substrate and cell-cell contacts (see Figures 11.13 and 11.14). The contraction of stress fibers produces tension across the cell, allowing the cell to pull on a substrate (e.g., the extracellular matrix) to which it is anchored. The contraction of adhesion belts alters the shape of epithelial cell sheets: a process that is particularly important during embryonic development, when sheets of epithelial cells fold into structures such as tubes.
The most dramatic example of actin-myosin contraction in nonmuscle cells, however, is provided by cytokinesisthe division of a cell into two following mitosis (Figure 11.27). Toward the end of mitosis in animal cells, a contractile ring consisting of actin filaments and myosin II assembles just underneath the plasma membrane. Its contraction pulls the plasma membrane progressively inward, constricting the center of the cell and pinching it in two. Interestingly, the thickness of the contractile ring remains constant as it contracts, implying that actin filaments disassemble as contraction proceeds. The ring then disperses completely following cell division.
Figure 11.27
Cytokinesis. Following completion of mitosis (nuclear division), a contractile ring consisting of actin filaments and myosin II divides the cell in two.
http://www.ncbi.nlm.nih.gov/books/NBK9961/
This is good. I don’t recall seeing it in the original comment. I am very aware of the actin myosin troponin connection in heart and in skeletal muscle, and I did know about the nonmuscle work. I won’t deal with it now, and I have been working with Aviral now online for 2 hours.
I have had a considerable background from way back in atomic orbital theory, physical chemistry, organic chemistry, and the equilibrium necessary for cations and anions. Despite the calcium role in contraction, I would not discount hypomagnesemia in having a disease role because of the intracellular-extracellular connection. The description you pasted reminds me also of a lecture given a few years ago by the Nobel Laureate that year on the mechanism of cell division.
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This is very insightful. There is no doubt that there is the bias you refer to. 42 years ago, when I was postdocing in biochemistry/enzymology before completing my residency in pathology, I knew that there were very influential mambers of the faculty, who also had large programs, and attracted exceptional students. My mentor, it was said (although he was a great writer), could draft a project on toilet paper and call the NIH. It can’t be true, but it was a time in our history preceding a great explosion. It is bizarre for me to read now about eNOS and iNOS, and about CaMKII-á, â, ã, ä – isoenzymes. They were overlooked during the search for the genome, so intermediary metabolism took a back seat. But the work on protein conformation, and on the mechanism of action of enzymes and ligand and coenzyme was just out there, and became more important with the research on signaling pathways. The work on the mechanism of pyridine nucleotide isoenzymes preceded the work by Burton Sobel on the MB isoenzyme in heart. The Vietnam War cut into the funding, and it has actually declined linearly since.
A few years later, I was an Associate Professor at a new Medical School and I submitted a proposal that was reviewed by the Chairman of Pharmacology, who was a former Director of NSF. He thought it was good enough. I was a pathologist and it went to a Biochemistry Review Committee. It was approved, but not funded. The verdict was that I would not be able to carry out the studies needed, and they would have approached it differently. A thousand young investigators are out there now with similar letters. I was told that the Department Chairmen have to build up their faculty. It’s harder now than then. So I filed for and received 3 patents based on my work at the suggestion of my brother-in-law. When I took it to Boehringer-Mannheim, they were actually clueless.
This is very insightful. There is no doubt that there is the bias you refer to. 42 years ago, when I was postdocing in biochemistry/enzymology before completing my residency in pathology, I knew that there were very influential mambers of the faculty, who also had large programs, and attracted exceptional students. My mentor, it was said (although he was a great writer), could draft a project on toilet paper and call the NIH. It can’t be true, but it was a time in our history preceding a great explosion. It is bizarre for me to read now about eNOS and iNOS, and about CaMKII-á, â, ã, ä – isoenzymes. They were overlooked during the search for the genome, so intermediary metabolism took a back seat. But the work on protein conformation, and on the mechanism of action of enzymes and ligand and coenzyme was just out there, and became more important with the research on signaling pathways. The work on the mechanism of pyridine nucleotide isoenzymes preceded the work by Burton Sobel on the MB isoenzyme in heart. The Vietnam War cut into the funding, and it has actually declined linearly since.
A few years later, I was an Associate Professor at a new Medical School and I submitted a proposal that was reviewed by the Chairman of Pharmacology, who was a former Director of NSF. He thought it was good enough. I was a pathologist and it went to a Biochemistry Review Committee. It was approved, but not funded. The verdict was that I would not be able to carry out the studies needed, and they would have approached it differently. A thousand young investigators are out there now with similar letters. I was told that the Department Chairmen have to build up their faculty. It’s harder now than then. So I filed for and received 3 patents based on my work at the suggestion of my brother-in-law. When I took it to Boehringer-Mannheim, they were actually clueless.