The levels of systemic arterial BP encountered in patients admitted for acute myocardial infarction (AMI) cover the gamut of values from hypertension (↑BP) to hypotension (↓BP). Also, the BP can either remain stable or show significant perturbations during the early phase of AMI. First, ↑BP can only be a manifestation of the clinical syndrome of AMI in patients without a history or evidence for ↑BP at subsequent follow-up. In this scenario, the patients are likely to have had an anterior AMI, have ↑BP, are sweating profusely, and manifest tachycardia, thus displaying the full complement of an autonomic hyperadrenergic state. These clinical features are transient, and BP in such patients is normal at follow-up. Second, BP can be high in patients with AMI and known or just-diagnosed ↑BP; often such a diagnosis can be made with certainty only at follow-up by documenting a persistently elevated BP. Third, BP in patients with an AMI can remain normal throughout the hospitalization, and at follow-up. Fourth, ↓BP can be seen along with evidence of tachycardia, and hypoperfusion of peripheral tissues in patients with cardiogenic shock.1–2 Some of these patients have ↓BP on admission or their initial BP is normal, prior to the development of ↓BP. Fifth, ↓BP may be observed in patients with inferior AMI and associated right ventricular infarct. In these patients ↓BP is mostly transient if fluids are infused in appropriate amounts, and its occurrence can be even prevented by such action. ST-segment elevation in right-chest ECG leads in patients with an inferior AMI,3–4 history of ↑ BP, and normal BP early after admission can aid in anticipating impending ↓BP.