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Nitro in ACS "Solving For X"

The majority of EMS protocols utilize a systolic stopping point for the administration of nitroglycerin in a patient with suspected ACS.
While not dumping their systolic pressure is important, I think an isolated focus on systole in a patient with ACS is the wrong move, and here's why..
A-orta-know this by now!
Let's start by reviewing how the coronary arteries are perfused. As the aortic valve opens and allows blood to eject from the left ventricle, blood will create a vortice around the aortic valve become present at the coronary ostia as seen in the illustration below.
I use to be under the impression that the reason the majority of myocardium perfused during diastole was due to the aortic valves physically covering up the coronary ostia. Vince DiGiulio (@MedicalApproach) from EMS12lead.com sent me some very compelling visual aids of the vortices that are created during left ventricular ejection. This can be seen if you watch a parasternal long's view of the aorta. The vortices become more pronounced as heart rate elevates as seen below.
Rather than obstruction of the coronary ostia being the reason for predominant myocardial diastolic perfusion, the real reason lies in the wall tension that takes place during systole. As the ventricles contract, the coronary arteries experience an increased resistance to forward flow. The same way cerebral perfusion would be compromised if the brain decided to contract a specific amount of times per minute. Knowing the right ventricle contracts with a lower pressure, we can understand why the heart receives perfusion during systole and diastole.
Coronary Perfusion Pressure
This brings us to the topic of coronary perfusion (cPP). To calculate cPP you subtract the pressure exerted against the wall of the ventricle from the diastolic pressure. In the example below you can see the diastolic blood pressure is 80 mmHg. If you were to float a catheter into the pulmonary artery, inflate the balloon to blind right sided influence, you would obtain a pressure of the left side of the heart during diastole. This pressure is known as the left ventricular end diastolic pressure (LVEDP).
A normal LVEDP can vary anywhere from 5 to 12 mmHg, and a normal cPP pressure is said to be anywhere between 60-80 mmHg. In the illustration above you can calculate a perfusion pressure of 68 mmHg, which is adequate.
Sooooo now that we got those fundamentals down.. what happens during an MI?
When coronary perfusion is compromised, depending on the geography and functional degree of infarction, the heart will experience a decrease in contractive force within the area of injury. This can be seen on an ultrasound as wall motion abnormality. Edema within the myocardium can create a decrease in compliance that elevates the LVEDP (Kobayashi, 2015). This loss in compliance can increase the wall tension to average of 19 mmHg with prognostic markers of heart failure when pressure exceed beyond 22mmHg.
Knowing that we have to subtract the wall tension pressure from our diastolic pressure to obtain a cPP, we can see the importance of avoiding a significant loss of diastolic pressure. The same principle we utilize when avoiding hypotension in patients with increased intracranial pressure in fear of dropping cerebral perfusion pressure beyond the gradient of the opposing pressure.
There is no strong literature to support the "ideal" diastolic pressure to maintain during ACS, but I believe 80 mmHg is something often referred to as a SWAG or scientific wild @ss guess (thanks @TheTotalEM).
Here is how I come up with 80ish..
1. If I subtract the average LVEDP during an MI of 19 mmHg from 80 mmHg, I still fall within an adequate perfusion pressure >60 mmHg.
2. The U shaped response to high and low diastolic pressures in patients after ACS shows a straight line between 70-90 mmHg (Bangalore, 2010)
3. A recent analysis from published in 2017 found a similar U shaped response in systolic and diastolic pressure. Exacerbation of ischemia was particular noticed when a drop in diastolic below 70 mmHg was noted (Park, 2017).
Regardless of the agent, it appears there is more risk in dropping the diastolic pressure than there is in allowing it to elevate. With paucity of literature supporting a mortality benefit for patients in ACS who receive nitroglycerin, I have utilized the following mental pathway of deciding on whether to use nitro AND analgesia, or strictly analgesia for the sole purpose of pain reduction.
Some will ask: "why even give nitroglycerin?" While a valid question, I do believe there may be some benefit in reducing pre-load, smoother muscle relaxation, and thus ventricular workload. Nitroglycerin requires an enzyme reaction to release nitric oxide from the endothelium. This enzyme is now known to be catalyzed within the mitochondria, which as you can imagine is very happy and welcoming during ischemia (EHHHHHHH). This may be the reason nitrate mortality benefit is higher with agents that do not need an enzymatic reaction to release nitric oxide (nitroprusside).
It important to consider that every patient comes with their own unique needs and titrations and that we are literally guessing wall tension pressure based off observational data. My purpose of this blog is to share the evidence I used to support a person mental model when treating patients with ACS. I believe morphine is not nearly as bad as everyone makes it out to be, but due to personal preference and current organizational stock, prefer the use of fentanyl. The argument of not treating ACS with analgesia for fear of a system that relies on patient discomfort to activate a cath-lab is not something I wish to address at this time.
Let's Break It Down!
1. I believe more attention should focus on diastolic pressure as a stopping point for vasodilators. It is within my best educated assumption that dropping a diastolic past 80 mmHg meets linear negative consequences to myocardial perfusion.
2.Fentanyl appears to only drop blood pressure as a reduction in catecholamine response to pain, and I am more likely to utilize this method as a mono-therapy as my diastolic approaches 80ish mmHg.
3.As far as the coronary dilation via nitroglycerin, I have conflicting view points on how much actually occurs when we are not directly introducing it into the coronary arteries. Because of the enzyme reaction that is needed to produce nitric oxide from nitroglycerin, it would appear that atherosclerosis would prevent absorption into the tunica intima.
References not hyperlinked are included below.
References
Bangalore S.,(2010). What Is the Optimal Blood Pressure in Patients After Acute Coronary Syndromes?
Relationship of Blood Pressure and Cardiovascular Events in the Pravastatin or Atorvastatin Evaluation and Infection Therapy–Thrombolysis in Myocardial Infarction (PROVE IT-TIMI) 22 Trial Originally published23 Nov 2010https://doi.org/10.1161/CIRCULATIONAHA.109.905687Circulation. 2010;122:2142–2151
Kobayashi, A., Misumida, N., Fox, J. T., & Kanei, Y. (2015). Prognostic Value of Left Ventricular End-Diastolic Pressure in Patients With Non-ST-Segment Elevation Myocardial Infarction. Cardiology research, 6(4-5), 301–305. doi:10.14740/cr406w
Park, H., Hong, Y. J., Cho, J. Y., Sim, D. S., Yoon, H. J., Kim, K. H., … Korean Acute Myocardial Infarction Registry Investigators (2017). Blood Pressure Targets and Clinical Outcomes in Patients with Acute Myocardial Infarction. Korean circulation journal, 47(4), 446–454. doi:10.4070/kcj.2017.0008
Original author: Tyler Christifulli
The majority of EMS protocols utilize a systolic stopping point for the administration of nitroglycerin in a patient with suspected ACS.
While not dumping their systolic pressure is important, I think an isolated focus on systole in a patient with ACS is the wrong move, and here's why..
A-orta-know this by now!
Let's start by reviewing how the coronary arteries are perfused. As the aortic valve opens and allows blood to eject from the left ventricle, blood will create a vortice around the aortic valve become present at the coronary ostia as seen in the illustration below.
I use to be under the impression that the reason the majority of myocardium perfused during diastole was due to the aortic valves physically covering up the coronary ostia. Vince DiGiulio (@MedicalApproach) from EMS12lead.com sent me some very compelling visual aids of the vortices that are created during left ventricular ejection. This can be seen if you watch a parasternal long's view of the aorta. The vortices become more pronounced as heart rate elevates as seen below.
Rather than obstruction of the coronary ostia being the reason for predominant myocardial diastolic perfusion, the real reason lies in the wall tension that takes place during systole. As the ventricles contract, the coronary arteries experience an increased resistance to forward flow. The same way cerebral perfusion would be compromised if the brain decided to contract a specific amount of times per minute. Knowing the right ventricle contracts with a lower pressure, we can understand why the heart receives perfusion during systole and diastole.
Coronary Perfusion Pressure
This brings us to the topic of coronary perfusion (cPP). To calculate cPP you subtract the pressure exerted against the wall of the ventricle from the diastolic pressure. In the example below you can see the diastolic blood pressure is 80 mmHg. If you were to float a catheter into the pulmonary artery, inflate the balloon to blind right sided influence, you would obtain a pressure of the left side of the heart during diastole. This pressure is known as the left ventricular end diastolic pressure (LVEDP).
A normal LVEDP can vary anywhere from 5 to 12 mmHg, and a normal cPP pressure is said to be anywhere between 60-80 mmHg. In the illustration above you can calculate a perfusion pressure of 68 mmHg, which is adequate.
Sooooo now that we got those fundamentals down.. what happens during an MI?
When coronary perfusion is compromised, depending on the geography and functional degree of infarction, the heart will experience a decrease in contractive force within the area of injury. This can be seen on an ultrasound as wall motion abnormality. Edema within the myocardium can create a decrease in compliance that elevates the LVEDP (Kobayashi, 2015). This loss in compliance can increase the wall tension to average of 19 mmHg with prognostic markers of heart failure when pressure exceed beyond 22mmHg.
Knowing that we have to subtract the wall tension pressure from our diastolic pressure to obtain a cPP, we can see the importance of avoiding a significant loss of diastolic pressure. The same principle we utilize when avoiding hypotension in patients with increased intracranial pressure in fear of dropping cerebral perfusion pressure beyond the gradient of the opposing pressure.
There is no strong literature to support the "ideal" diastolic pressure to maintain during ACS, but I believe 80 mmHg is something often referred to as a SWAG or scientific wild @ss guess (thanks @TheTotalEM).
Here is how I come up with 80ish..
1. If I subtract the average LVEDP during an MI of 19 mmHg from 80 mmHg, I still fall within an adequate perfusion pressure >60 mmHg.
2. The U shaped response to high and low diastolic pressures in patients after ACS shows a straight line between 70-90 mmHg (Bangalore, 2010)
3. A recent analysis from published in 2017 found a similar U shaped response in systolic and diastolic pressure. Exacerbation of ischemia was particular noticed when a drop in diastolic below 70 mmHg was noted (Park, 2017).
Regardless of the agent, it appears there is more risk in dropping the diastolic pressure than there is in allowing it to elevate. With paucity of literature supporting a mortality benefit for patients in ACS who receive nitroglycerin, I have utilized the following mental pathway of deciding on whether to use nitro AND analgesia, or strictly analgesia for the sole purpose of pain reduction.
Some will ask: "why even give nitroglycerin?" While a valid question, I do believe there may be some benefit in reducing pre-load, smoother muscle relaxation, and thus ventricular workload. Nitroglycerin requires an enzyme reaction to release nitric oxide from the endothelium. This enzyme is now known to be catalyzed within the mitochondria, which as you can imagine is very happy and welcoming during ischemia (EHHHHHHH). This may be the reason nitrate mortality benefit is higher with agents that do not need an enzymatic reaction to release nitric oxide (nitroprusside).
It important to consider that every patient comes with their own unique needs and titrations and that we are literally guessing wall tension pressure based off observational data. My purpose of this blog is to share the evidence I used to support a person mental model when treating patients with ACS. I believe morphine is not nearly as bad as everyone makes it out to be, but due to personal preference and current organizational stock, prefer the use of fentanyl. The argument of not treating ACS with analgesia for fear of a system that relies on patient discomfort to activate a cath-lab is not something I wish to address at this time.
Let's Break It Down!
1. I believe more attention should focus on diastolic pressure as a stopping point for vasodilators. It is within my best educated assumption that dropping a diastolic past 80 mmHg meets linear negative consequences to myocardial perfusion.
2.Fentanyl appears to only drop blood pressure as a reduction in catecholamine response to pain, and I am more likely to utilize this method as a mono-therapy as my diastolic approaches 80ish mmHg.
3.As far as the coronary dilation via nitroglycerin, I have conflicting view points on how much actually occurs when we are not directly introducing it into the coronary arteries. Because of the enzyme reaction that is needed to produce nitric oxide from nitroglycerin, it would appear that atherosclerosis would prevent absorption into the tunica intima.
References not hyperlinked are included below.
References
Bangalore S.,(2010). What Is the Optimal Blood Pressure in Patients After Acute Coronary Syndromes?
Relationship of Blood Pressure and Cardiovascular Events in the Pravastatin or Atorvastatin Evaluation and Infection Therapy–Thrombolysis in Myocardial Infarction (PROVE IT-TIMI) 22 Trial Originally published23 Nov 2010https://doi.org/10.1161/CIRCULATIONAHA.109.905687Circulation. 2010;122:2142–2151
Kobayashi, A., Misumida, N., Fox, J. T., & Kanei, Y. (2015). Prognostic Value of Left Ventricular End-Diastolic Pressure in Patients With Non-ST-Segment Elevation Myocardial Infarction. Cardiology research, 6(4-5), 301–305. doi:10.14740/cr406w
Park, H., Hong, Y. J., Cho, J. Y., Sim, D. S., Yoon, H. J., Kim, K. H., … Korean Acute Myocardial Infarction Registry Investigators (2017). Blood Pressure Targets and Clinical Outcomes in Patients with Acute Myocardial Infarction. Korean circulation journal, 47(4), 446–454. doi:10.4070/kcj.2017.0008
Original author: Tyler Christifulli

The majority of EMS protocols utilize a systolic stopping point for the administration of nitroglycerin in a patient with suspected ACS.
While not dumping their systolic pressure is important, I think an isolated focus on systole in a patient with ACS is the wrong move, and here's why..
A-orta-know this by now!
Let's start by reviewing how the coronary arteries are perfused. As the aortic valve opens and allows blood to eject from the left ventricle, blood will create a vortice around the aortic valve become present at the coronary ostia as seen in the illustration below.
I use to be under the impression that the reason the majority of myocardium perfused during diastole was due to the aortic valves physically covering up the coronary ostia. Vince DiGiulio (@MedicalApproach) from EMS12lead.com sent me some very compelling visual aids of the vortices that are created during left ventricular ejection. This can be seen if you watch a parasternal long's view of the aorta. The vortices become more pronounced as heart rate elevates as seen below.
Rather than obstruction of the coronary ostia being the reason for predominant myocardial diastolic perfusion, the real reason lies in the wall tension that takes place during systole. As the ventricles contract, the coronary arteries experience an increased resistance to forward flow. The same way cerebral perfusion would be compromised if the brain decided to contract a specific amount of times per minute. Knowing the right ventricle contracts with a lower pressure, we can understand why the heart receives perfusion during systole and diastole.
Coronary Perfusion Pressure
This brings us to the topic of coronary perfusion (cPP). To calculate cPP you subtract the pressure exerted against the wall of the ventricle from the diastolic pressure. In the example below you can see the diastolic blood pressure is 80 mmHg. If you were to float a catheter into the pulmonary artery, inflate the balloon to blind right sided influence, you would obtain a pressure of the left side of the heart during diastole. This pressure is known as the left ventricular end diastolic pressure (LVEDP).
A normal LVEDP can vary anywhere from 5 to 12 mmHg, and a normal cPP pressure is said to be anywhere between 60-80 mmHg. In the illustration above you can calculate a perfusion pressure of 68 mmHg, which is adequate.
Sooooo now that we got those fundamentals down.. what happens during an MI?
When coronary perfusion is compromised, depending on the geography and functional degree of infarction, the heart will experience a decrease in contractive force within the area of injury. This can be seen on an ultrasound as wall motion abnormality. Edema within the myocardium can create a decrease in compliance that elevates the LVEDP (Kobayashi, 2015). This loss in compliance can increase the wall tension to average of 19 mmHg with prognostic markers of heart failure when pressure exceed beyond 22mmHg.
Knowing that we have to subtract the wall tension pressure from our diastolic pressure to obtain a cPP, we can see the importance of avoiding a significant loss of diastolic pressure. The same principle we utilize when avoiding hypotension in patients with increased intracranial pressure in fear of dropping cerebral perfusion pressure beyond the gradient of the opposing pressure.
There is no strong literature to support the "ideal" diastolic pressure to maintain during ACS, but I believe 80 mmHg is something often referred to as a SWAG or scientific wild @@ss guess (thanks @TheTotalEM).
Here is how I come up with 80ish..
1. If I subtract the average LVEDP during an MI of 19 mmHg from 80 mmHg, I still fall within an adequate perfusion pressure >60 mmHg.
2. The U shaped response to high and low diastolic pressures in patients after ACS shows a straight line between 70-90 mmHg (Bangalore, 2010)
3. A recent analysis from published in 2017 found a similar U shaped response in systolic and diastolic pressure. Exacerbation of ischemia was particular noticed when a drop in diastolic below 70 mmHg was noted (Park, 2017).
Regardless of the agent, it appears there is more risk in dropping the diastolic pressure than there is in allowing it to elevate. With paucity of literature supporting a mortality benefit for patients in ACS who receive nitroglycerin, I have utilized the following mental pathway of deciding on whether to use nitro AND analgesia, or strictly analgesia for the sole purpose of pain reduction.
Some will ask: "why even give nitroglycerin?" While a valid question, I do believe there may be some benefit in reducing pre-load, smoother muscle relaxation, and thus ventricular workload. Nitroglycerin requires an enzyme reaction to release nitric oxide from the endothelium. This enzyme is now known to be catalyzed within the mitochondria, which as you can imagine is very happy and welcoming during ischemia (EHHHHHHH). This may be the reason nitrate mortality benefit is higher with agents that do not need an enzymatic reaction to release nitric oxide (nitroprusside).
It important to consider that every patient comes with their own unique needs and titrations and that we are literally guessing wall tension pressure based off observational data. My purpose of this blog is to share the evidence I used to support a person mental model when treating patients with ACS. I believe morphine is not nearly as bad as everyone makes it out to be, but due to personal preference and current organizational stock, prefer the use of fentanyl. The argument of not treating ACS with analgesia for fear of a system that relies on patient discomfort to activate a cath-lab is not something I wish to address at this time.
Let's Break It Down!
1. I believe more attention should focus on diastolic pressure as a stopping point for vasodilators. It is within my best educated assumption that dropping a diastolic past 80 mmHg meets linear negative consequences to myocardial perfusion.
2.Fentanyl appears to only drop blood pressure as a reduction in catecholamine response to pain, and I am more likely to utilize this method as a mono-therapy as my diastolic approaches 80ish mmHg.
3.As far as the coronary dilation via nitroglycerin, I have conflicting view points on how much actually occurs when we are not directly introducing it into the coronary arteries. Because of the enzyme reaction that is needed to produce nitric oxide from nitroglycerin, it would appear that atherosclerosis would prevent absorption into the tunica intima.
References not hyperlinked are included below.
References
Bangalore S.,(2010). What Is the Optimal Blood Pressure in Patients After Acute Coronary Syndromes?
Relationship of Blood Pressure and Cardiovascular Events in the Pravastatin or Atorvastatin Evaluation and Infection Therapy–Thrombolysis in Myocardial Infarction (PROVE IT-TIMI) 22 Trial Originally published23 Nov 2010https://doi.org/10.1161/CIRCULATIONAHA.109.905687Circulation. 2010;122:2142–2151
Kobayashi, A., Misumida, N., Fox, J. T., & Kanei, Y. (2015). Prognostic Value of Left Ventricular End-Diastolic Pressure in Patients With Non-ST-Segment Elevation Myocardial Infarction. Cardiology research, 6(4-5), 301–305. doi:10.14740/cr406w
Park, H., Hong, Y. J., Cho, J. Y., Sim, D. S., Yoon, H. J., Kim, K. H., … Korean Acute Myocardial Infarction Registry Investigators (2017). Blood Pressure Targets and Clinical Outcomes in Patients with Acute Myocardial Infarction. Korean circulation journal, 47(4), 446–454. doi:10.4070/kcj.2017.0008
Original author: Tyler Christifulli

The majority of EMS protocols utilize a systolic stopping point for the administration of nitroglycerin in a patient with suspected ACS.
While not dumping their systolic pressure is important, I think an isolated focus on systole in a patient with ACS is the wrong move, and here's why..
A-orta-know this by now!
Let's start by reviewing how the coronary arteries are perfused. As the aortic valve opens and allows blood to eject from the left ventricle, blood will create a vortice around the aortic valve become present at the coronary ostia as seen in the illustration below.
I use to be under the impression that the reason the majority of myocardium perfused during diastole was due to the aortic valves physically covering up the coronary ostia. Vince DiGiulio (@MedicalApproach) from EMS12lead.com sent me some very compelling visual aids of the vortices that are created during left ventricular ejection. This can be seen if you watch a parasternal long's view of the aorta. The vortices become more pronounced as heart rate elevates as seen below.
Rather than obstruction of the coronary ostia being the reason for predominant myocardial diastolic perfusion, the real reason lies in the wall tension that takes place during systole. As the ventricles contract, the coronary arteries experience an increased resistance to forward flow. The same way cerebral perfusion would be compromised if the brain decided to contract a specific amount of times per minute. Knowing the right ventricle contracts with a lower pressure, we can understand why the heart receives perfusion during systole and diastole.
Coronary Perfusion Pressure
This brings us to the topic of coronary perfusion (cPP). To calculate cPP you subtract the pressure exerted against the wall of the ventricle from the diastolic pressure. In the example below you can see the diastolic blood pressure is 80 mmHg. If you were to float a catheter into the pulmonary artery, inflate the balloon to blind right sided influence, you would obtain a pressure of the left side of the heart during diastole. This pressure is known as the left ventricular end diastolic pressure (LVEDP).
A normal LVEDP can vary anywhere from 5 to 12 mmHg, and a normal cPP pressure is said to be anywhere between 60-80 mmHg. In the illustration above you can calculate a perfusion pressure of 68 mmHg, which is adequate.
Sooooo now that we got those fundamentals down.. what happens during an MI?
When coronary perfusion is compromised, depending on the geography and functional degree of infarction, the heart will experience a decrease in contractive force within the area of injury. This can be seen on an ultrasound as wall motion abnormality. Edema within the myocardium can create a decrease in compliance that elevates the LVEDP (Kobayashi, 2015). This loss in compliance can increase the wall tension to average of 19 mmHg with prognostic markers of heart failure when pressure exceed beyond 22mmHg.
Knowing that we have to subtract the wall tension pressure from our diastolic pressure to obtain a cPP, we can see the importance of avoiding a significant loss of diastolic pressure. The same principle we utilize when avoiding hypotension in patients with increased intracranial pressure in fear of dropping cerebral perfusion pressure beyond the gradient of the opposing pressure.
There is no strong literature to support the "ideal" diastolic pressure to maintain during ACS, but I believe 80 mmHg is something often referred to as a SWAG or scientific wild @ss guess (thanks @TheTotalEM).
Here is how I come up with 80ish..
1. If I subtract the average LVEDP during an MI of 19 mmHg from 80 mmHg, I still fall within an adequate perfusion pressure >60 mmHg.
2. The U shaped response to high and low diastolic pressures in patients after ACS shows a straight line between 70-90 mmHg (Bangalore, 2010)
3. A recent analysis from published in 2017 found a similar U shaped response in systolic and diastolic pressure. Exacerbation of ischemia was particular noticed when a drop in diastolic below 70 mmHg was noted (Park, 2017).
Regardless of the agent, it appears there is more risk in dropping the diastolic pressure than there is in allowing it to elevate. With paucity of literature supporting a mortality benefit for patients in ACS who receive nitroglycerin, I have utilized the following mental pathway of deciding on whether to use nitro AND analgesia, or strictly analgesia for the sole purpose of pain reduction.
Some will ask: "why even give nitroglycerin?" While a valid question, I do believe there may be some benefit in reducing pre-load, smoother muscle relaxation, and thus ventricular workload. Nitroglycerin requires an enzyme reaction to release nitric oxide from the endothelium. This enzyme is now known to be catalyzed within the mitochondria, which as you can imagine is very happy and welcoming during ischemia (EHHHHHHH). This may be the reason nitrate mortality benefit is higher with agents that do not need an enzymatic reaction to release nitric oxide (nitroprusside).
It important to consider that every patient comes with their own unique needs and titrations and that we are literally guessing wall tension pressure based off observational data. My purpose of this blog is to share the evidence I used to support a person mental model when treating patients with ACS. I believe morphine is not nearly as bad as everyone makes it out to be, but due to personal preference and current organizational stock, prefer the use of fentanyl. The argument of not treating ACS with analgesia for fear of a system that relies on patient discomfort to activate a cath-lab is not something I wish to address at this time.
Let's Break It Down!
1. I believe more attention should focus on diastolic pressure as a stopping point for vasodilators. It is within my best educated assumption that dropping a diastolic past 80 mmHg meets linear negative consequences to myocardial perfusion.
2.Fentanyl appears to only drop blood pressure as a reduction in catecholamine response to pain, and I am more likely to utilize this method as a mono-therapy as my diastolic approaches 80ish mmHg.
3.As far as the coronary dilation via nitroglycerin, I have conflicting view points on how much actually occurs when we are not directly introducing it into the coronary arteries. Because of the enzyme reaction that is needed to produce nitric oxide from nitroglycerin, it would appear that atherosclerosis would prevent absorption into the tunica intima.
References not hyperlinked are included below.
References
Bangalore S.,(2010). What Is the Optimal Blood Pressure in Patients After Acute Coronary Syndromes?
Relationship of Blood Pressure and Cardiovascular Events in the Pravastatin or Atorvastatin Evaluation and Infection Therapy–Thrombolysis in Myocardial Infarction (PROVE IT-TIMI) 22 Trial Originally published23 Nov 2010https://doi.org/10.1161/CIRCULATIONAHA.109.905687Circulation. 2010;122:2142–2151
Kobayashi, A., Misumida, N., Fox, J. T., & Kanei, Y. (2015). Prognostic Value of Left Ventricular End-Diastolic Pressure in Patients With Non-ST-Segment Elevation Myocardial Infarction. Cardiology research, 6(4-5), 301–305. doi:10.14740/cr406w
Park, H., Hong, Y. J., Cho, J. Y., Sim, D. S., Yoon, H. J., Kim, K. H., … Korean Acute Myocardial Infarction Registry Investigators (2017). Blood Pressure Targets and Clinical Outcomes in Patients with Acute Myocardial Infarction. Korean circulation journal, 47(4), 446–454. doi:10.4070/kcj.2017.0008
Original author: Tyler Christifulli
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