According to the latest statistics from the American Heart Association, about 16.5 million Americans over the age of 20 currently suffer from some form of coronary heart disease. Every five minutes, 14 Americans will have an acute coronary event, and nine of those will be myocardial infarctions. Every 39 seconds, one American will die from this (AHA Statistics Committee and Stroke Statistics Subcommittee 2012).
Emergency medical service personnel will treat about 62 percent of those sudden deaths (Chugh et al. 2004).
The conditions that ultimately result in these acute coronary events begin in the coronary arteries. In a process that usually takes several decades, fatty materials such as cholesterol accumulate between the lining of the artery and the surrounding arterial muscle layer to form a substance known as plaque. As the plaque builds, the arterial lumen narrows, thereby reducing blood flow through the area.
In some cases, the plaque cap ruptures, setting in motion a series of events that produce a localized blood clot called a thrombus. Every one of the acute coronary syndromes begins with this plaque rupture (Brogan 2002).
The growing thrombus further restricts blood flow through the affected coronary artery. The heart muscle downstream becomes hypoxic, creating a pain sensation for the patient. If the thrombus completely occludes the artery, the downstream myocardium will be in serious trouble.
It is very important, then, to stop the growth of the developing clot quickly and dissolve or remove the remaining obstruction in order to save as much heart muscle as possible.
Not every plaque rupture results in a completely occluded coronary artery or myocardial infarction. There are three different types of acute coronary syndromes (AHA 2001). The exact syndrome that exists in your patient depends upon the amount of heart muscle affected and the degree of coronary artery occlusion.
Physical exam alone cannot provide enough diagnostic information for differentiating between any of the acute coronary syndromes because their presentations are quite similar (Karve, Bossone and Mehta 2007).
However, subtle changes in a patient’s electrocardiogram reflect the degree of tissue deterioration and will help to identify the most serious and time-sensitive subset of acute coronary syndromes, the ST-segment elevation myocardial infarction (STEMI). This ECG pattern reflects conditions that place sections of the heart muscle at great risk of cellular death if the medical team does not quickly restore adequate perfusion.
Patients who receive definitive reperfusion therapy within 70 minutes of symptom onset have more than a 50 percent reduction in infarction size and a 75 percent reduction in mortality (Brouwer et al. 1996).
Experts recommend that patients suffering from a blocked coronary artery should receive coronary angioplasty when the door-to balloon time is less than 90 minutes (O’Connor et al. 2010).
Door-to-balloon time
The door-to-balloon time is typically defined as the interval from when the patient first arrives in the emergency department encounters until balloon inflation in a catheterization lab (Antman et al. 2004). Every 30-minute increase in door-to-balloon time results in a one-year mortality increase of 7.5 percent (De Luca, Suryapranata, Ottervanger and Antman 2004).
Primary angioplasty involves threading a balloon catheter through the vasculature until reaching the site of obstruction. The cardiologist can advance a guide wire through the thrombus for precise placement of the empty balloon.
Once the balloon is correctly located, the cardiologist can inflate it with water, usually at pressures many times greater than normal blood pressure. The inflating balloon compresses the plaque against the artery wall, which reestablishes blood flow through the affected artery often to greater than 90 percent of normal blood flow (Topol 1996). After deflating the balloon, the cardiologist can insert a metal scaffold, or stent, into that section of the artery to maintain lumen patency.
Reaching door-to-balloon goals
One factor that makes achieving the door-to-balloon goal possible is to have the emergency department notify and activate the catheterization lab while the patient is en route (Eckstein, Koenig, Kaji and Tadeo 2009).
To help achieve that goal, experts recommend that EMS systems take an active role in early identification of patients suffering from myocardial infarction by providing prehospital 12-lead electrocardiograms (National Heart Attack Alert Program Coordinating Committee, 60 Minutes to Treatment Working Group 1994).
Acquisition of the 12-lead ECG increases the on-scene time interval by an average of no more than four minutes but results in earlier primary angioplasty by 23 minutes compared to patients with emergency department-acquired first ECGs (Canto et al. 1997). Data currently suggests that patients who undergo emergent percutaneous coronary intervention fare better at high-volume rather than low-volume hospitals (Kimmel, Berlin and Laskey 1995).
Experts often emphasize the time-sensitivity of coronary revascularization with the phrase, “time is muscle” (Gibson, C. M., de Lemos, J. A., Antman, E. M. and the TIMI Study Group 2004, Time is muscle in primary PCI: the strength of the evidence grows. European Heart Journal, 25(12), 1001-1002. doi: 10.1016/j.ehj.2004.04.029).
Patients who suffer myocardial infarction in the out-of-hospital environment have better outcomes when the medical community works together to minimize the time before the patient gets to a catheterization lab.
Proven methods for reducing the important door-to-balloon time include prehospital acquisition of a 12-lead ECG, early recognition of the electrical pattern associated with infarction and early notification of the emergency department and catheterization team.
References
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