**2. The following case serves to illustrate the result of AMI usual treatment at present**

52-year-old male, with grade II obesity, dyslipidemia, hypertension, and smoking history and with no previous cardiovascular events, arrives at the hospital 60 minutes after the onset of symptoms. The first electrocardiogram (ECG) shows rS in V1, V2, and V3 and ST-segment elevation from V1 to V6 (**Figure 1**).

At admission the arterial blood pressure was 145/80 mm of hg, the heart rate was 78 beats per minute, and the Killip Kimball grade was A. The patient received aspirin (250 mg), clopidogrel (600 mg), unfractionated heparin in intravenous bolus (5000 UI), and rosuvastatin (40 mg). At 80 minutes after admission, 140 minutes from the onset of symptoms, coronary angiography is performed showing single-vessel disease with thrombotic occlusion of the middle third of the anterior descending artery (ADA) and TIMI 0 flow. Primary angioplasty is performed to the middle third of the ADA with thromboaspiration and stent implantation achieving an adequate result with TIMI 3 flow, symptom relief, and absence of complications.

**245**

**Figure 3.** *ECG at 48 hours.*

*Primary Angioplasty: From the Artery to the Myocardium*

The post-procedure ECG shows QS in V1, V2, and V3 and ST level and negative T

IECA and B blockers are started. It evolves without recurrence of symptoms; however, at 48 hours, the ECG shows QS from V1 to V5 and low R in V6 (**Figure 3**). Note that despite early assistance, it no longer has positive vectors in V1, V2, and V3, and after the usual successful treatment and aligned with the guidelines based on current evidence, it continues to lose precordial vectors after primary angioplasty. The echocardiogram shows antero-apical dyskinesia and impaired ventricular function, with an ejection fraction of 35% measured by the Simpson method. There are several mechanisms by which the myocardium is lost in the

*DOI: http://dx.doi.org/10.5772/intechopen.91832*

from V1 to V6 (**Figure 2**).

*ECG postprimary angioplasty.*

**Figure 2.**

different phases of AMI.

**Figure 1.** *ECG at admission.*

*Primary Angioplasty: From the Artery to the Myocardium DOI: http://dx.doi.org/10.5772/intechopen.91832*

*Cardiac Diseases - Novel Aspects of Cardiac Risk, Cardiorenal Pathology and Cardiac Interventions*

contributed to improving early and late artery permeability [15, 16]. The enormous effort focused on the treatment of the coronary artery has led to the fact that the success of primary angioplasty is now greater than 95% [7]. The angiographic success rate ceased to be a problem. However, the post-AMI incidence of death and heart failure remains around 20% during the first year [17], and as mentioned earlier this correlates directly with the amount of myocardium damaged and the

**2. The following case serves to illustrate the result of AMI usual** 

rS in V1, V2, and V3 and ST-segment elevation from V1 to V6 (**Figure 1**).

52-year-old male, with grade II obesity, dyslipidemia, hypertension, and smoking history and with no previous cardiovascular events, arrives at the hospital 60 minutes after the onset of symptoms. The first electrocardiogram (ECG) shows

At admission the arterial blood pressure was 145/80 mm of hg, the heart rate was 78 beats per minute, and the Killip Kimball grade was A. The patient received aspirin (250 mg), clopidogrel (600 mg), unfractionated heparin in intravenous bolus (5000 UI), and rosuvastatin (40 mg). At 80 minutes after admission, 140 minutes from the onset of symptoms, coronary angiography is performed showing single-vessel disease with thrombotic occlusion of the middle third of the anterior descending artery (ADA) and TIMI 0 flow. Primary angioplasty is performed to the middle third of the ADA with thromboaspiration and stent implantation achieving an adequate result with TIMI 3 flow, symptom relief, and absence of complications.

deterioration of ventricular function.

**treatment at present**

**244**

**Figure 1.** *ECG at admission.* The post-procedure ECG shows QS in V1, V2, and V3 and ST level and negative T from V1 to V6 (**Figure 2**).

IECA and B blockers are started. It evolves without recurrence of symptoms; however, at 48 hours, the ECG shows QS from V1 to V5 and low R in V6 (**Figure 3**).

Note that despite early assistance, it no longer has positive vectors in V1, V2, and V3, and after the usual successful treatment and aligned with the guidelines based on current evidence, it continues to lose precordial vectors after primary angioplasty. The echocardiogram shows antero-apical dyskinesia and impaired ventricular function, with an ejection fraction of 35% measured by the Simpson method. There are several mechanisms by which the myocardium is lost in the different phases of AMI.

**Figure 3.** *ECG at 48 hours.*
