Heart Attack

A heart attack, or myocardial infarction (MI), is permanent damage to the heart muscle. It affects millions of people worldwide each year. Current therapeutic treatments are mainly used for the prevention but not the post-treatment of heart attack. They do nothing to protect the heart muscle cells from death after heart attack. Therefore, we developed several potent drug candidates (peptide 2 and 3) that can be used as an effective post-treatment to stop the cell death signaling pathway in heart muscle cells after heart attack. Both peptide 2 and 3 are water soluble and membrane permeable. Post-treatment with our lead compound (i.v. injection, 20mg/kg) effectively restored heart function in a rat model of heart attack compared with the saline-treated group.

Table 1. Therapeutic efficacy of the 3 peptides in restoring rat heart function after acute myocardial infarction

Groups HR SBP LVSP LVEDP +dp/dtmax -dp/dtmax
Per min mmHg mmHg mmHg mmHg/s mmHg/s
Sham 395±36.1 121±15.2 143±22.3 3.31±2.00 8522±892 -6317±2537
Saline 390±24.7 110±13.4 130±12.4 21.0±4.51 4501±1535 -3365±750
Peptide 1 395±41.8 111±22.1 128±13.9 19.0±5.77 4443±1493 -3431±1110
Peptide 2 406±16.1 121±14.6 139±8.59 13.0±4.03** 8324±1353*** -5686±1436**
Peptide 3 393±38.8 123±13.8 155±8.02*** 9.41±4.25*** 8222±872*** -5885±573***

**p﹤0.01,*** p﹤0.001 VS the saline group.

Data are presented as Mean±SD

 

HR: heart rate;

SBP: Systolic blood pressure;

LVSP: left ventricular systolic pressure;

LVEDP: left ventricular end diastolic pressure;

±dp/dtmax: The rate (dP/dt max) of left ventricle (LV) pressure rise in early systole is  one of

the oldest measures of LV global contractility. The greater the contractile force exerted, the

greater the rate of increase in left ventricular pressure.