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At age 28? I don’t think so. I’m not obese and have no other health issues, saving near-sightedness and having a cold at the moment.

Young is the worst age to have them. You haven't had enough years to develop the collateral circulation that lessens the impact of an infarction. For young people, the first sign of a heart attack is usually sudden death.

As far as a cold is concerned, look at this:

Blood Coagul Fibrinolysis. 2007 Dec;18(8):713-8.

Inflammatory changes during the 'common cold' are associated with platelet activation and increased reactivity of platelets to agonists.

Kreutz RP, Tantry US, Bliden KP, Gurbel PA.
Sinai Center for Thrombosis Research,
Baltimore, Maryland 21215, USA.

Epidemiologic studies have shown increased rates of myocardial infarction after upper respiratory tract infections. We hypothesized that changes in platelet activation and reactivity and inflammation occur during the 'common cold'. Previously healthy individuals with viral upper respiratory tract infections were studied (n = 18). Venous blood samples were obtained during the time of infection and again after 6 weeks. Platelet reactivity was higher during the 'common cold' as measured by low-dose ADP-induced aggregation (46 +/- 28 versus 27 +/- 21% 6 weeks after presentation, P = 0.003) and was higher than control individuals (22 +/- 8%, P = 0.003). Platelet P-selectin expression increased during illness (2.3 +/- 0.2% CD62-positive platelets versus 1.8 +/- 0.1% at 6 weeks after presentation, P = 0.017; and 1.7 +/- 0.2% in the control group, P = 0.03). C-reactive protein (3.7 +/- 1.3 versus 2.2 +/- 1.5 mg/l, P = 0.004) and tumor necrosis factor-alpha (27.6 +/- 28 versus 12.7 +/- 9 pg/ml, P = 0.03) were increased during the 'common cold'. There were no significant differences in levels of soluble P-selectin (P = 0.18), soluble vascular adhesion molecule-1 (P = 0.59) and soluble intercellular adhesion molecule-1 (P = 0.23). Increased platelet reactivity and activation during the 'common cold' are associated with inflammation as measured by increased levels of C-reactive protein and tumor necrosis factor-alpha, but not increased levels of endothelial markers. These findings support a pro-aggregatory state that, in part, explains the thrombotic events shown by epidemiological studies.